Auricular  Flutter 


W.T.  Ritchie 


KC6  8d"  -^  -K^\ 
Columbia  Banibersiitp  . 
in  m  Citp  of  i^etD  gorfe  ^"^f 

College  o(  ^fjpgicianss  anli  ^urgeong 


department  of  $J)psiiolosp 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/auricularflutterOOritc 


AURICULAR     FLUTTER 


CVlQyLlIiSVRRRTECREPOill 


PRINTED   BY 

CPvEEN     AND     SON 

Kn  IN  BURGH 


May  l!:il4. 


AURICULAR    FLUTTER 


BY 

WILLIAM   THOMAS    RITCHIE 

iM.D.,  F.R.C.P.E.,  F.R.S.E. 

rUVSICIAN    TO   THE    DEACONESS   HOSPITAL;    ASSISTANT   PHYSICIAN   TO   THE    ROYAL    INKIKMARY  ; 

LECTURER  ON  THE  PRACTICE  OK  MEDICINE,  SCHOOL  OF  MEDICINE  OF  THE  ROYAL  C0LLE0E8  ; 

LECTURER   ON    CLINICAL   MEDICINE   IN   THE   UNIVERSITY   OF   EIJINBUROH 


^ 


NEW    YORK 
PAUL    B.    HOEBER 

PUBLISHER 


CoPN  \ 


PREFACE 

jModkkn  luetliod.s  of  elinieal  iiivestigatiuii  have  arinnk'il  iniicli  iiilniina- 
tioii  leganliiig  the  natiiie  and  the  causes  of  heart  failure.  This  grave, 
and  often  fatal,  event  is  now  recognised  as  heing  not  inrre(|uently  a 
result  of  disease  of  the  auricles. 

In  order  to  understand  the  nature  and  signiticance  of  the  disorders 
of  the  auricles,  a  preliminary  account  is  given  of  certain  facts  concern- 
ing the  anatomy  and  physiology  of  the  heart,  the  pulsations  of  the 
jugular  veins  and  the  electrocardiogram. 

The  disturbances  of  the  cardiac  action  that  are  due  to  extrasystoles 
and  auricular  fibrillation,  and  their  relation  to  allied  disorders,  are  dis- 
cussed in  the  first  chapter.  The  subsequent  chapters  deal  with  that 
condition  of  extreme  acceleration  of  the  auricles  which  is  known  as 
auricular  fiutter.  The  physiological,  pathological,  and  clinical  facts 
regarding  this  disorder,  and  the  features  which  distinguish  it  from 
other  disturbances  of  the  heart's  action,  are  described. 

All  the  illustrations,  with  two  exceptions,  have  been  obtained  from 
cases  that  have  come  under  my  own  observation.  To  the  Edlnhurgh 
Medical  Journal,  to  the  Clarendon  Press,  and  to  the  publishers  of 
HQart,  I  am  indebted  for  permission  to  reproduce  illustrations. 

My  sincere  acknowledgments  are  rendered  to  my  colleagues  in 
the  Pioyal  Infirmary,  and  especially  to  Professor  William  Paissell  and 
Dr.  Lovell  Gulland,  for  their  generous  permission  to  examine  and 
record  the  cases  under  their  charge.  To  John  Cowan,  George  D. 
Mathewson,  and  Theodore  Shennan  I  am  indebted  for  much  kind 
assistance  in  the  preparation  of  this  work.  I  have  to  thank  "VV.  E. 
Hume  and  George  D.  Mathewson  for  allowing  me  to  reproduce  the 
records  in  Figs.  ^'1  and  80,  and  W.  Stevens  for  his  skilled  assistance 
in  obtaining  most  of  the  electrocardiograms. 


VI 


PREFACE 


For  the  facilities  afforded  me  for  the  investigation  of  cases  I 
cordially  express  my  indebtedness  to  the  Trustees  of  the  Clinical 
Medicine  Eesearch  Laboratory  of  the  Royal  Infirmary  and  to  the 
Laboratory  Committee  of  the  Eoyal  College  of  Physicians  of 
Edinburgh. 


Edinburgh, 
May  1914. 


CONTENTS 

CHAPTER  I 
INTRODUCTION 

PAOF.S 

The  Simis  Node.  The  Atrio-ventricukr  Conducting  System.  The  Pulsa- 
tions of  llie  JuguUir  Veins.  Tlie  Electrocardiograni.  Extrasystolcs. 
Auricular  Fibrillation      .  .  .  .  .  .1-23 

CHAPTER  n 

ETIOLOGY 

The  E.xperimental  Production  of  Auricular  Flutter.  Auricular  Flutter 
combined  with  Fibrillation.  Influence  of  the  Nervous  System.  Age. 
Sex.      Arterial  Disease.      Heart  Disease.      Other  Etiological  Factors         24-29 

CHAPTER   HI 

MORBID   ANATOMY 

The    Pathological    Condition    of   the    Heart   in    Six    Cases   of   Auricular 

Flutter      .........         30-34 

CHAPTER  IV 

RECORDS   OF   CASES 

Clinical  and  Graphic  Records  of  Eleven  Cases  under  Personal  Observa- 
tion, and  Forty-two  other  Cases  recorded  in  the  Literature .  .         35-80 

CHAPTER  V 

CLINICAL  FEATURES 

Auricular  Flutter  in  an  Apparently  Healthy  Heart.  Auricular  Flutter 
Supervening  during  the  Course  of  Chronic  Heart  Disease.  Auricular 
Flutter  with  Partial  Heart-block.  Auricular  Flutter  with  Complete 
Heart-block  ........         81-89 

CHAPTER  VI 
GRAPHIC  RECORDS 

Sphygraograms.     Jugulo-carotid  Tracings.     Electrocardiograms    .  .         90-94 


viii  CONTENTS 

CHAPTER   VII 
THE  ACTION  OF  THE  VAGUS  AND  SYMPATHETIC 

PAGES 

I.  The  Action  of  the  Vagus  on  the  Heart  with  a  Physiological  Rhythm — 
Effects  on  the  Auricles,  on  the  At rio- ventricular  Conducting  System, 
and  on  the  Ventricles.  After-effects  of  Vagus  Stimulation.  II.  The 
Action  of  the  Sympathetic  on  the  Normal  Heart.  III.  The  Action 
of  the  Vagus  in  Auricular  Flutter.  IV.  The  Action  of  the  Sympa- 
thetic in  Auricular  Flutter  ......       95-105 

CHAPTER   VIII 

THE  ACTION  OF  DRUGS  OF  THE  DIGITALIS  GROUP 

I.  Digitalis — Ventricular  Retardation,  Auricular  Fibrillation,  Restoration 
of  the  Normal  Rhythm.  II.  Strophanthus.  III.  Squill.  Similarity 
of  Effects  to  those  of  Vagus  Stimulation  ....     106-110 

CHAPTER  IX 

DIAGNOSIS 

I.  Physiological  Rhythm  without  Acceleration.  II.  Sinus  Tachycardia. 
III.  Extrasystolic  Arrhythmia.  IV.  Nodal  Rhythm  and  Paroxysmal 
Tachycardia.     V.  Auricular  Fibrillation  ....     111-125 

CHAPTER  X 

PROGNOSIS 

Restoration  of  Normal  Rhythm.  Recurrent  Attacks.  Persistent  Flutter. 
Death.  Significance  of  Alternation,  Chronic  Valvular  Disease,  and 
Myocarditis  .  .  .  .  .  .  .  .126-128 

CHAPTER   XI 

TREATMENT 

Treatment   during  an  Attack — Rest,  Diet,    Drugs.      Treatment   of   the 

Causal  Condition.     Prevention  of  Recurrent  Attacks  .  .     129-133 

General  Index         ........     135-141 

Index  of  Authors    ,  ,  ,  ,  ,  .  .     142-144 


LIST    OF    ILLUSTRATIONS 

111  all  the  elect roi'jinliogiaius,  except  those  in   Figs.  32  ami  89,  the  time  recoi-d 
is  28"57  per  second,     lu  all  the  polygraph  tracings  the  time  record  is  0*2  second. 


1.  Horizontal    section    through    the    right   nuricle,    showing  the  .sinus  nod 

(Plate  I.)      .  .      ' 

2.  Nerve  with  ganglion  cells  near  the  sinus  node.     (Plate  I.)    . 

3.  The  atrio-ventricular  bundle.     (Plate  II.)      .... 

4.  The  atrio-ventricular  bundle  and  its  branches.     (Plate  III.) 

5.  Normal  jugulo-carotid  and  brachial  tracings  .... 

6.  Normal  jugulo-carotid  and  brachial  tracings  . 

7.  Sinus  arrhythmia  with  h  waves  in  the  jugulo-carotid  tracing 

8.  Electrocardiographic  control  curves    ..... 

9.  Normal  electrocardiogram        ...... 

10.  Jugulo-carotid  pulsations  and  electrocardiogram 

11.  Monophasic  and  diphasic  deflexions    ..... 

12.  Electrocardiograms  in  mitral  stenosis  and  in  aortic  incompetence    . 

1 3.  Brachial  and  apical  tracings  showing  an  extrasystole 

1 4.  Sphygmogram.     An  extrasystole  with  a  fully  compensatory  pause 

15.  Sphygmogram.     An  extrasystole  that  does  not  cause  a  pulse-wave  . 

16.  Sphygmogram.     An  extrasystole  followed  by  an  incomplete  pause 

17.  Electrocardiograms.     Ventricular  extrasystoles.     (Plate  IV.) 

18.  Sphygmogram    and     electrocardiogram.      An    interpolated    extrasystole, 

(Plate  V.)    . 

19.  Electrocardiograms.     Ventricular  extrasystoles  of  type  1.     (Plate  V.) 

20.  Electrocardiograms.     Ventricular  extrasystoles  of  type  2.     (Plate  V.) 

21.  Electrocardiogram.     Auricular  extrasystoles.     (Plate  VI.)    . 

22.  Syphilitic  aortitis.     (Plate  VI.)  ..... 

23.  Orthodiagram.     Normal  heart  ..... 

24.  Orthodiagram.     Mitral  stenosis  and  auricular  fibrillation     . 

25.  Orthodiagram.     Auricular  fibrillation  .... 

26.  Tracings  from  a  case  of  auricular  fibrillation .... 

27.  Electrocardiogram  from  a  case  of  auricular  fibrillation 

28.  Inflammatory  infiltration  of  the  auricular  muscle  in  Case  III. 

29.  Orthodiagram  in  Case  I.  .....  . 

30.  Tracings  showing  complete  heart-block  .... 

31.  Tracings.     Auricular  flutter  and  complete  heart-block 

32.  Electrocardiogram.      Auricular  flutter  and  complete  heart-block.      (Plate 

VII.) 

33.  Electrocai'diogiam.    Auricular  flutter,  complete  heart-block,  and  one  veiitri 

cular  extrasystole.     (Plate  VII.)     ..... 

34.  Electrocardiogram  after  cessation  of   auricular  flutter  in  Case  I.     (Plate 

VII.)  .  .  .  .  .  .  . 

35.  Electrocardiogram.     Compression  of  the  left  vagus  in  auricular  lluLter  an 

complete  heart-block.     (Plate  VIII.)  .... 


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42 

42 

42 

42 


X  LIST   OF   ILLUSTEATIOXS 

FIG.  PAGE 

36.  Electrocardiogram.     Auricular  flutter  and  complete  heart-block.     Deriva- 

tion I.     (Plate  IX.)  ....... 

37.  Electrocardiogram.     Auricular  flutter  and  complete  heart-block.     Deriva- 

tion I.     (Plate  IX.)  ....... 

38.  Electrocardiogram.     Aui-icidar  flutter  and  complete  heart-block.     Deriva- 

tion II.     (Plate  IX.)  ....... 

39.  Electrocardiogram.     Auricular  flutter  and  complete  heart-block.     Deriva- 

tion II.     (Plate  IX.)  ....... 

40.  Electrocardiogram.     Auricular  flutter  and  complete  heart-block.     Deriva- 

tion III.     (Plate  IX.) 

41.  Electrocardiogram.     Auricular  flutter  and  complete  heart-block.     Deriva- 

tion III.     (Plate  IX.) 

42.  Tracings  showing  group-beating  of  the  ventricles  in  Case  I. 

43.  Tracings.     Auricular  flutter  with  a  ventricular  response  to  every  second 

auricular  beat  ...... 

44.  Tracings.     Auricular  flutter  with  irregular  ventricular  responses 

45.  Tracings.     Auricular  flutter  with  grouping  of  the  ventricular  beats 

46.  Electrocardiogram.     Auricular  flutter  with  a  ventricular  response  to  every 

second  auricular  beat.     (Plate  X.)  ..... 

47.  Electrocardiogram.     Auricular  flutter  with  a  ventricular  response  to  every 

fourth  ventricular  beat.     (Plate  X.)  . 

48.  Electrocardiogram.     Auricular  fibrillation.     Case  II.     (Plate  X.)  . 

49.  Tracings.      Auricular  flutter   with   a  pulse-rate   one-fourth   that   of  the 

auricles         .  .  .  .  .  .  . 

50.  Orthodiagram.     Case  II.  . 

51.  Tracings.     Auricular  flutter  with  a  pulse-rate  of  159'5  per  minute 

52.  Electrocardiogi'am.       Auricular     flutter.       Case     III.        Derivation     I. 

(Plate  XL) 

53.  Electrocardiogram.       Auricular     flutter.       Case     III.       Derivation     II. 

fPlate  XL)  ......... 

54.  Electrocardiogram.       Auricular    flutter.       Case     III.       Derivation     III. 

(Plate  XL) 

55.  Electrocardiogram.     Auricular  filuillation  after  strophanthin.     Case  III. 

(Plate  XL) 

56.  Electrocardiogram.       Xormal      rhythm.       Case      III.       Derivation      I. 

(Plate  XL)  .  .  .         " 

57.  Electrocardiogram.       Xormal     rlivthm.       Case      III.       Derivation     II. 

(Plate  XL)   .  .  .         \ 

58.  Electrocardiogram.       Xormal     rhvthm.      Case     III.       Derivation     III. 

(Plate  XL)  .  .  .         '    . 

59.  Electrocardiogram.       Auricular      flutter.       Case     lY.       Derivation     II. 

(Plate  XII.) 

■60.  Electrocardiogram.  Xormal      rhythm.       Case       IV.       Derivation      I. 

(Plate  XIL) 

61.  Electrocardiogram.  Xormal     rhythm.        Case     IV.      Derivation      II. 

(Plate  XIL)  ........ 

€2.  Electrocardiogram.  Xormal     rhythm.       Case      IV.       Derivation     III. 

(Plate  XII.)  .  .        '     . 

63.  Electrocardiogram.  Auricular     flutter.       Case     XL       Derivation     II. 

(Plate  XIL) 

64.  Electrocardiogram.      Auricular     flutter.      Case     XL      Derivation     III. 

(Plate  XIL) 


LIST   OF   ILLUSTKATIONS  xi 


FIO. 

65.  Brachial  i)iil.sati(iii.s  and  I'lectnxardioj^iaiu.     Auririilar  llutler.    Conipres 

siou  of  the  li^'ht  va<,Mis.     (Plate  XIII.)    .... 

66.  Tracings.     Auricular  Mutter  at  a  rate  of  350  i)er  minute    . 

67.  Tracings.     Auricular  tihrillation.     Case  VI. 

68.  Tracings.     Sinus  irregularity  and  extrasytoles.     Case  VII. 

69.  Tracings.     Rhythmic  tachycardia  with  alternating  pulse.     Case  VII, 

70.  Tracing  of  the  pulsations  of  the  abdominal  aorta.     Case  VII. 

71.  Tracings.     Ehythmic  tachycardia  at  a  rate  of  225  per  minute 

72.  Tracings.     Rhythmic  tachycardia  at  a  rate  of  131  per  minute 

73.  Electrocardiogram.     Com]ilete  heart-block  .... 

74.  Sphygmograms  in  auricular  thitter  ..... 

75.  Sphygmograms  in  auricular  flutter,  with  grouping  of  the  judse-beats 

76.  Tracings.     Auricular  llutler,  with  ventricular  responses  to  every  second 

or  third  beat  ...... 

77.  Tracings.     Auricular  flutter  at  a  rate  of  196  per  miniite     . 

78.  Tracings.     Auricular  flutter  at  a  rate  of  266  per  minute     . 

79.  Electrocardiogram.     Auricular  flutter,  with  an  auriculo-ventricular  ratio 

of  2:1.     (Plate  XIV.) 

80.  Electrocardiogram.     Auricular  Hutter,  with  an  auriculo-ventricular  ratio 

of  3  : 1  (G.  D.  Mathewson).     (Plate  XIV.) 

81.  Electrocardiogram.     Auricular  flutter,  with  an  auriculo-ventricular  ratio 

of  4:1.     (Plate  XIV.)       ..... 

82.  Electrocardiogram.     Auricular  flutter  with  irregular  ventricular  responses 

(Plate  XV.) 

83.  Sphygmograni  and  electrocardiogram.     Auricular  flutter  and  fibrillation 

combined.     (Plate  XV.)    ...... 

84.  Electrocardiogram.     Compression  of  the  right  vagus.     (Plate  XVI.) 

85.  Electrocardiogram.     Compression  of  the  right  vagus.     (Plate  XVI.) 

86.  Diagram.     Auricular  acceleration  after  atropin 

87.  Diagram.     The  effects  of  atropin  in  a  case  of  digitalis  heart-block 

88.  Electrocardiogram.     Compression  of  the  right  vagus  causing  heart-block 

(Plate  XVII.) ' 

89.  Electrocardiogram.     Slow  difference  of  potential  upon  compression  of  the 

right  vagus.     (Plate  XVII.)  ..... 

90.  Tracing.     Alternating  pulse  after  vagus  compression 

91.  Electrocardiogram.     The  effect  of  vagus  compression  in  auricular  flutter 

Case  II.,    (Plate  XVIII.) 

92.  Tracing  from  cat's  auricle.     Faradisation  of  auricle  and  stimulation  of  the 

vagus  (W.  E.  Hume)  ..... 

93.  Tracings.     Sinus  tachycardia  .... 

94.  Diagrams  showing  simulation  of  extrasystoles  by  ventricular  irregularity 

in  flutter    ....... 

95.  Electrocardiogram.     Sinus  tachycardia.     (Plate  XIX.) 

96.  Electrocardiogram.     Multiple  extrasystoles.     (Plate  XIX.) 

97.  Electrocardiogram.     Auricular  flutter  with  irregular  ventricular  responses, 

(Plate  XIX.) 

98.  Tracings.     Paroxy.smal  tachycardia  due  to  ventricular  extrasystoles 

99.  Tracings.     Nodal  rhythm     ..... 

100.  Electrocardiogram.     Nodal  arrhythmia.     (Plate  XX.) 

101.  Electrocardiogram.     Nodal  rhythm.     (Plate  XX.)  . 

102.  Electrocardiogram.     Auricular  fibrillation.     (Plate  XX.)    . 

103.  Tracings  from  a  case  of  paroxysmal  tachycardia 


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61 
61 
63 
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92 
92 

92 

92 

92 

94 

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102 

104 

109 
113 

114 
114 
114 

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115 
118 
120 
120 
120 
122 


xii  LIST   OF   ILLUSTEATIONS 

FIG.  PACE 

104.  Sphygmogram  showing  grouping  of  the  pulse-beats  in  auricular  flutter. 

Case  V.       .  .  .  .  .  .  .  .  .124 

10.5.  Electrocardiogram.      Auricular  fibrillation  passing  into  flutter.     (Plate 

XXI.) 124 

106.  Sphygmogram  and  electrocardiogram.     Auricular  flbrillation  passing  into 

flutter.     (Plate  XXI.)        .  .  .  .  .  .  .124 

107.  Tracings.     Auricular  flutter  with  irregular  arterial  pulse  .  .  .     125 


AUKlCrLAR    FLUTTER 


CHAPTER  I 

INTRODUCTION 

Nearly  all  our  knowledge  of  the  action  of  the  auricles  in  disease  has 
been  acquired  within  recent  years.  It  is  true  that  the  pulsations  of 
the  veins  in  the  neck  had  been  described  by  Galen  ^  and  by  ]\Iorgagni  - ; 
nevertheless,  in  the  middle  of  the  last  century,  Stokes  ^  admitted  that 
"  although  in  most  cases  of  dilatation  of  the  heart  we  find  the  auricles, 
as  well  as  the  ventricles,  engaged,  yet  our  knowledge  of  the  disease  as 
afiecting  the  former  cavities  is  very  limited."  He  added  that  "  fortu- 
nately this  is  not  of  much  consequence  to  practical  medicine."  Graphic 
records  of  the  venous  pulsations  in  the  neck  were  obtained  by  Bamberger,^ 
Geigel,°  and  Marey^in  1863,  and  by  Friedreich "  in  1866.  Riegel^in 
1881  described  certain  features  which  were  considered  to  distinguish 
the  normal  from  the  pathological  venous  pulse ;  and  in  Gibson's  ^  paper 
in  1882  all  the  important  facts  that  were  then  known  regarding  the 
action  of  the  auricles  in  health  and  disease  were  discussed. 

The  publication  of  Mackenzie's  ^'^  monograph  in  1902  inaugurated  a 

^  Galen,  quoted  by  ^lorgagni. 

'  Morgagni,  J.  B.,  De  sedibus  et  causis  morhorum,  Venetiis,  1762,  lib.  i.,  Epist. 
anat.  med.,  xviii.,  art.  9,  10,  11. 

2  Stokes,  "W.,  TJie  Diseases  of  the  Heart  and  the  Aorta,  Dublin,  1854,  273. 

*  Bamberger,  H.,  "Beobachtungen  liber  den  Venenpuls,"  JFurzburger  med.  Zeitschr.,. 
Wiirzburg,  1863,  iv.  232. 

^  Geigel,  A.,  "Ueber  den  Yenenpuls,"  ibid.,  1863,  iv.,  332. 

"  Marey,  E.  .J.,  Physiologie  medicale  de  la  circulation  du  sang,  Paris,  1863, 
530-532. 

"  Friedreicb,  X.,  "Ueber  den  Venenpuls,"  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 
1866,  i.,  241. 

*  Riegel,  F.,  ''Zur  Kenntniss  von  dem  Verlialten  des  Yenensystems  unter 
normalen  luid  pathologischen  Yerhtiltuissen,"  Berl.  klin.  IVochenschr.,  1881,  xviii., 
249. 

"  Gibson,  G.  A.,  "The  Action  of  tlie  Auricles  in  Health  and  Disease,"  Edin.  Med, 
Journ.,  1882,  xxviii.,  118. 

i"  Mackenzie,  J.,  Tlie  Study  of  the  Pulse,  Edin.  and  Lond.,  1902. 

1 


2  INTEODUCTION 

new  era  in  our  knowledge  of  the  diseases  of  the  heart.  He  showed  how 
the  jugular  pulsations  could  be  analysed  with  precision  and  accuracy, 
and  moreover  he  proved  that  a  careful  analysis  of  tracings  from  these 
veins  was  of  great  clinical  importance  in  determining  the  mechanism 
of  the  heart's  action  in  health  and  disease.  By  means  of  the  methods 
which  Mackenzie  introduced,  an  accurate  clinical  study  of  the  auricles 
was,  for  the  first  time,  rendered  possible. 

The  next  striking  advance  in  our  knowledge  of  the  disorders  of  the 
heart's  action  was  made  by  Wenckebach^  in  1903.  By  a  critical 
analysis  of  sphymographie  tracings  he  demonstrated  that  each  form 
■of  cardiac  irregularity  represented  a  disorder  of  one  or  other  of  the 
functional  activities  of  the  heart,  namely,  of  stimulus  production,  excita- 
bility, contractility,  and  conductivity.  This  interpretation  of  the  cardiac 
arrhythmias  was  adopted  and  amplified  by  Mackenzie^  in  1908,  and  is 
now  generally  accepted. 

The  deeper  insight  that  was  gained  by  Mackenzie's  methods  of 
studying  the  heart  disclosed  the  fact  that  many  cardiac  problems 
required  re-investigation  from  the  standpoint  of  anatomy,  physiology, 
pathology,  and  therapeutics.  Some  of  these  problems  have  apparently 
been  solved,  while  others  still  await  elucidation.  Within  the  last 
decade  the  most  notable  advance  in  the  study  of  the  heart  has  been 
effected  by  the  introduction  of  Einthoven's  ^  string  galvanometer.  By 
means  of  this  instrument,  as  well  as  by  the  methods  introduced  by 
Mackenzie,  it  is  now  possible  to  study  the  action  of  the  heart  with  a 
precision  that  was  formerly  unattainable,  and  the  prognosis  and  treat- 
ment of  cases  of  heart  disease  have  consequently  been  placed  on  a 
more  rational  and  scientific  basis. 


The  Sinus  Node 

The  "primitive  tissue"  in  the  auricular  walls  of  the  mammalian 
heart  represents,  according  to  Keith  and  Flack,*   the  remains  of   the 

1  Wenckebach,  K.  F.,  Die  Arhythmie  ah  Ausdruck  bestimmter  Fimktionsstorungen 
des  Herzens,  Leipz.,  1903  ;  and  English  translation  by  Snowball,  T,,  Edin.,  1904. 

2  Mackenzie,  J.,  Diseases  of  the  Heart,  Lond.,  1908. 

2  Einthoven,  W.,  "Ein  neues  Galvanometer,"  Annalend.  Physik,  Lei-pz.,  1903, 
4  Eolge,  xii.,  1059.  See  also  papers  in  Onderzoekingen  gedaan  in  het  physiologisch 
Laboratorium  der  Universiteit  te  Leiden,  Tweede  Reeks,  v.,  vi. 

*  Keith,  A.,  and  Flack,  M.,  "  The  Form  and  Nature  of  the  Muscular  Connections 
between  the  Primary  Divisions  of  the  Vertebrate  Heart,"  Journ.  of  Anat.  and  Physiol., 
Loud.,  1907,  xli.,  172. 


I'LATK   I. 


Fin.  1.— Horizontal  section  (X  2  diameters)  thiongli  the  right 
amide  near  its  .junction  witli  the  superior  vena  cava.  A,  the 
inter-auricular  septum  ;  li,  right  auricular  appendix  tilled  with 
thrombi ;  '/,  connective  tissue  in  which  there  are  many  large 
nerves.  I>,  the  sinus  node,  in  the  right  posterior  asjiect  of  the 
auricular  wall,  is  demarcated  by  the  lines  di-awn  around  it. 


Fig.  2. — Xeire  with  ganglion  cells  near  the  sinns  node.  Lymphocytic 
infiltration  of  the  connective  tissue.  Auricular  flutter,  Case  III. 
( X  100  diameters.) 


THE   COXDUCTING   SYSTEM  3 

sinus  venosus.  This  tissue  may  be  found  close  to  the  mouths  of  the 
puhnonaiy  veins  and  coronary  sinus,  and  at  one  area  where  it  is 
especially  abundant  it  constitutes  the  sinus,  or  sino-auricular,  node. 
This  has  the  form  of  an  elongated  spindle,  about  2-2*5  cm,  in  length 
and  2  mm.  in  breadth,  which  lies  in  the  sub-epicardial  tissue  at  the 
junction  of  the  superior  vena  cava  with  the  right  auricular  appendix 
(Fig.  1).  The  long  axis  of  the  node  is  parallel  with  the  sulcus  termin- 
alis.  If  a  section,  in  the  long  axis  of  the  superior  vena  cava,  be  made 
through  the  cavo-auricular  junction,  the  small  artery  running  in  the 
long  axis  of  the  node  is  seen  in  oblique  or  transverse  section. 

The  sinus  node  consists  of  an  irregular  meshwork  of  slender  muscle 
fibres,  with  definite  transverse  striation,  embedded  in  somewhat  com- 
pact connective  tissue.  These  muscle  fibres  are  in  direct  continuity 
with  the  adjacent  muscle  fibres  of  the  auricular  wall.  AVithin  the  node, 
and  running  in  its  long  axis,  is  the  small  artery  already  mentioned.  In 
the  vicinity  of  the  node  and  elsewhere  at  the  cavo-auricular  junction 
there  are  abundant  nerves  and  ganglia  (Fig.  2).  Some  of  the  former 
pass  into  the  node,  but  Miss  Meiklejohn  ^  found  no  nerve  endings  in  the 
sinus  node  of  man  comparable  to  those  in  the  sinus  node  of  the  monkey. 
The  sinus  node  is  generally  held  to  set  the  pace  and  rhythm  of  the 
normal  heart,  and  it  is  believed  to  be  mainly  through  this  node  that 
vagus  and  sympathetic  influences  reach  the  auricles. 

The  Atrio-yentpjcular  Coxductixg  System 

The  system  whereby  stimuli  are  conducted  from  the  sinus  node  and 
the  auricles  to  the  ventricles  consists  of  a  node,  and  a  bundle  with  two 
branches  and  their  terminal  ramifications. 

The  airio-ventricalar  node,-  measuring  about  2*7  by  1'7  mm.,  lies  in 
the  right  lateral  aspect  of  the  auricular  septum,  in  front  of  the  mouth 
of  the  coronary  sinus  and  above  the  posterior  end  of  the  septal  cusp 
of  the  tricuspid' valve.  This  node,  like  the  sinus  node,  consists  of  an 
irregular  meshwork  of  slender  striated  muscle  fibres,  but  the  amount 
of  intervening  connective  tissue  is  less  abundant.  At  the  posterior 
extremity  of  the  node  its  slender  muscle  fibres  gradually  merge  in  the 
larger  muscle  fibres  of  the  auricular  septum.  A  small  artery  usually 
passes  forwards  into  the  node. 

'  Meiklejohn,  J.,  "  On  the  Innervation  of  the  Xodal  Tissue  of  the  Mammalian 
Heart,"  Journ.  of  Anat.  and  Physiol.,  Loud.,  1914,  xlviii.,  1. 

-  Tawara,  S.,  Das  Reideitungssystem  des  Saugetierhenens,  Jena,  1908. 


4  INTEODUCTION 

The  atrio-ventricular  hvMdle,^  which  is  about  1*5  mm.  in  diameter, 
consists  mainly  of  a  somewhat  regular  network  of  slender  striated 
muscle  fibres.  It  arises  from  the  anterior  extremity  of  the  node  and 
passes  downwards,  forwards,  and  to  the  left,  until  it  reaches  the  lowest 
part  of  the  pars  membranacea  septi  (Plates  II.  and  III.),  where  it 
divides.  The  atrio-ventricular  node  and  bundle  of  man  differ  from 
those  of  most  other  mammalia  in  possessing  a  very  scanty  nerve  supply. 
Miss  Meiklejohn  -  was  able  to  demonstrate  a  few  small  nerve  fibres,  but 
no  nerve  plexus  or  nerve  endings. 

The  left  branch  of  the  bundle  remains  on  the  left  side  of  the 
ventricular  septum,  and  as  its  fibres  pass  downwards  they  spread  out 
fanwise  in  the  sub-endocardial  tissue.  The  right  branch,  which  is 
usually  of  ovoid  or  cylindrical  form  on  transverse  section,  passes  down- 
wards and  to  the  right  until  it  lies  in  the  sub-endocardial  tissue  on  the 
right  side  of  the  ventricular  septum.  The  right  branch  ultimately 
passes  on  to  the  moderator  band  of  the  right  ventricle. 

The  terminal  ramifications  of  both  branches — the  Purkinje  fibres 
— run  in  the  sub-endocardial  tissue,  and  eventually  merge  with  the 
ventricular  muscle  fibres.  The  Purkinje  fibres  which  have  the  shortest 
course  are  those  passing  to  the  papillary  muscles  of  the  two  ventricles. 

By  means  of  this  system,  stimuli  from  the  sinus  or  auricles  are 
transmitted  to  both  ventricles  simultaneously,  and  as  the  papillary 
muscles  are  the  first  to  receive  each  stimulus,  they  begin  to  contract 
before  the  main  mass  of  ventricular  muscle. 


The  Pulsations  of  the  Jugulae  Veins 

The  rate  and  rhythm  of  the  auricular  contractions  in  health  can 
usually  be  ascertained  with  considerable  accuracy  by  careful  inspection 
of  the  pulsations  in  the  jugular  veins.  If  the  patient  be  in  the 
recumbent  posture,  with  his  head  low,  gentle  pulsation  of  the  internal 
jugular  vein  is  usually  visible  in  the  lower  part  of  the  neck,  and  is  more 
distinct  on  the  right  than  on  the  left  side.  In  health,  even  although 
venous  pulsation  of  considerable  amplitude  be  seen,  it  cannot  be  felt 
when  a  finger  is  applied  lightly  over  the  vein,  whereas  firmer  pressure 

1  Kent,  A.  F.  S.,  "  Researches  on  the  Structure  and  Function  of  tlie  Mammalian 
Heart,"  Journ.  of  Physiol,  Canib.,  1893,  xiv.,  233.  His,  W.,  Jr.,  "Die  Thatigkeit  des 
embryonalen  Herzens  und  deren  Bedeutung  fiir  die  Lehre  A'on  der  Herzbewegung 
beim  Erwachsenen,"  Arheiten  a.  d.  med.  Klinik,  Leipz.,  1893,  14. 

2  Meiklejohn,  J.,  lac.  cit. 


I'LATK   II. 


SrctiotI 
.No.  143. 


Xo.  203. 


No.  •22!". 


_^A 


Fio.  .3. — Sdial  sections  in  the  liorizontal  plane  of  the  septum  of 
a  liealtliy  liiimaii  lieart,  illustniting  tlie  ori^iin,  position,  and 
course  of  the  atrio-ventricujar  bundle.  The  sections  were 
treated  with  van  Gieson's  stain  ;  the  fibrous  tissue  conse- 
quently appears  dark,  the  muscle  ti.ssue  pale,  (x  4.)  (Edin. 
Med.  j'nuni.,  I'.iOO,  vol.  ii.) 


I'LA  I'l',   III. 


Section 
No.  245. 


Xo.  247. 


No.  2.53. 


Xo.  2.59. 


Fk;.  4. — Fnrtlie-r  .seetion.s  from  tlio  .same  heart  as  depicted  in 
Plate  11.,  to  show  the  bifurcation  of  the  atrio-ventriciilar 
bundle  and  its  two  msiin  branches,  (x  4.)  (Kdin.  ^fc(l. 
Jovrn.,  WOO,  vol.  ii.) 


THE  JUGULAR   PULSATIONS  5 

will  enable  the  pulsation  of  the  adjacent  carotid,  ov  subclavian,  artery 
to  l)e  felt. 

If  the  pulsations  on  the  right  side  of  the  neck  are  watched,  and 
if  sinniltaneously  their  time  relation  to  the  apex-beat,  the  sounds  of 
the  heart  or  the  carotid  pulse  on  the  left  side,  is  noted,  two  or  three 
impulses  may  be  seen  in  the  jugular  vein  for  each  beat  of  the  ventricles. 
If  only  two  impulses  can  be  seen,  the  first  is  found  to  be  ventriculo- 
systolic  in  time,  for  it  appears  to  be  synchronous  with  the  apex-beat, 
the  first  sound  of  the  heart  or  the  carotid  in)pulse,  whereas  the  second 
impulse  in  the  jugular  vein  occurs  simultaneously  with  or  immediately 
after  the  second  sound,  and  is  therefore  ventriculo-diastolic  in  time.  If 
a  third  impulse  be  visible  in  the  veins,  it  is  seen  to  occur  immediately 
before  the  first  sound  of  the  heart  is  heard,  and  is  therefore  a  pre-systolic 
impulse. 


brachial 
Fig.  5. — Xormaljugulo-carotid  pulsations.    The  time  record  is  0'2  second. 

The  pulsations  in  the  vessels  of  the  neck  can  be  analysed  with 
greater  accuracy  and  precision  if  simultaneous  tracings  are  taken  from 
the  jugular  vein  and  from  the  apex -beat  or  the  arterial  pulse  in  the 
arm.  The  most  serviceable  instrument  for  this  purpose  is  Mackenzie's  ^ 
polygraph,  which  enables  two  tracings  to  be  taken  simultaneously,  and 
also  gives  a  time  record  in  fifths  of  a  second.  Each  rise  of  pressure  in 
the  auricles  and  in  the  jugular  veins  is  represented  by  a  rise  on  the 
jugulo-carotid  tracing,  whereas  each  fall  of  pressure  within  the  auricles 
or  great  veins  results  in  a  depression  of  the  tracing.  Thus  with  each 
inspiration  the  intra-auricular  pressure  falls  and  the  line  of  the  tracing 
descends  slowly ;  during  each  expiration  the  pressure  in  the  auricles 
rises  and  the  line  of  the  tracing  ascends  gradually.  In  addition  to 
these  slow  respiratory  undulations,  the  tracing  presents  a  series  of 
quicker  waves  and  depressions  representing  changes  of  pressure  within 
the  auricles  during  each  cardiac  cycle. 

1  Mackenzie,  .J.,  Diseases  of  tlie  Heart,  third  edition,  Lond.,  1913,  105-108. 


6  INTRODUCTIONS^ 

In  analysing  the  jugular  tracing,  the  time  relation  of  its  various 
waves  and  depressions  to  the  events  recorded  in  the  arterial,  or  apical, 
tracing  should  be  determined  hj  means  of  careful  measurement  from 
the  ordinates.  It  is  then  possible  to  ascertain  the  time  in  the  cardiac 
cycle  at  which  each  wave  or  depression  upon  the  jugular  tracing  occurs. 
For  example,  in  the  upper  tracing  of  Fig.  6  the  wave  c  begins 
0'06  second  before  the  commencement  of  the  arterial  pulse-wave  in  the 
lower  tracing,  and  represents  the  carotid  impulse  transmitted  to  the 
jugular  vein.  Following  the  carotid  wave  there  is  a  depression  re. 
This  is  due  partly  to  auricular  relaxation,  but  also  to  the  fact  that 
during  the  early  phase  of  ventricular  systole  the  papillary  muscles, 
pulling  upon  the  auricles,  enlarge  these  chambers  and  consequently 
lower  the  pressure  within  them,  even  although  the  auriculo-ventricular 
valves  are  closed.     Towards  the  end  of  ventricular  systole  the  intra- 


FiG.  G. — Xormal  rhythm.     Jugulo-carotid  and  brachial  tracings. 

auricular  pressure  again  rises,  and  the  line  of  the  jugular  curve  ascends 
gradually,  so  as  to  constitute  the  wave  r.  The  pressure  within  the 
auricles  and  great  veins  continues  to  rise  until  the  auriculo-ventricular 
valves  open.  This  event  is  represented  in  the  tracing  by  the  summit 
of  the  wave  v.  The  intra-auricular  pressure  then  falls  rapidly,  as  shown 
by  the  depression  y,  and  thereafter  the  pressure  rises  slowly  while  both 
the  auricles  and  the  ventricles  become  filled  with  blood.  About  one- 
tenth  of  a  second  before  ventricular  systole,  the  auricles  contract  and 
the  pressure  within  the  auricles  is  notably  increased.  This  is  repre- 
sented by  the  wave  a  in  the  jugular  tracing. 

The  interval  between  the  auricular  and  the  carotid  waves  (the  a-c 
interval)  is  appreciably  longer  than  the  auriculo-ventricular  interval 
(As—  Vs  =  0'14:  second)  because  of  the  pre-sphygmic  period  and  the 
time  required  for  the  transmission  of  the  pulse- wave  from  the  aortic 
orifice  to  the  arteries  of  the  neck.  In  health  the  a-c  interval  is  about 
0'17  second.     Pathological  prolongation  of   the  a-c  interval  exceeding 


THE   ELECTKOCAKDTOGRAM 


0*2  second  may  be  due  to  (1)  delay  in  the  trausinissioii  of  the  stimulus 
from  auricle  to  ventricle ;  (2)  lengthening  of  the  pre-sphygmic  period  ; 
(3)  unduly  slow  transmission  of  the  arterial  pulse  wave;  or  (4)  any  of 
these  factors  conjointly. 

Although  the  nornuxl  jugulo-carotid  tracing  usually  presents  three 
waves  a,  c,  and  r  in  succession,  certain  other  waves  may  be  observed 
even  when  the  heart  is  beating  with  a  physiological  rhythm. 

(1)  A  small  wave,  h,  may  occasionally  be  seen  interposed  between 
the  waves  a  and  c.  It  probably  represents  an  impulse  transmitted  to 
the  blood  within  the  auricle  at  the  moment  when  the  tricuspid  valve 
closes  early  in  systole. 

(2)  The  wave  r  may  be  represented  by  two  summits,  v^  and  t'-. 
The  notch  or  depression  between  them  coincides  approximately  either 


.4^^ 


^C 


yv_ 


yx^ 


^rdu-Zu^. 


Fig.  7. — Sinus  arrhj-thmia  with  h  waves  in  tlie  .jugtilo-carotid  tracing.    From  a  case  of  duodenal  ulcer 

with  healthy  heart. 

with  the  end  of  ventricular  systole  or  with  the  closure  of  the  semi- 
lunar valves. 

(3)  The  wave  h  (Fig.  7),  which  was  first  described  by  Hirschfelder  ^ 
and  A.  G.  Gibson,-  occurs  in  mid-diastole,  and  is  ascribed  to  the  apposi- 
tion of  the  segments  of  the  tricuspid  valve  when  the  ventricle  becomes 
filled  by  the  inrush  of  blood  from  the  auricle.  The  interval  between 
this  wave  and  the  antecedent  carotid  wave  is  constant  for  each  individual 
patient.  The  h  wave  may  be  accompanied  by  an  audible  third  heart 
sound. 


The  Electeocaediogram 

Whenever  a  muscle  or  other  excitable  tissue  is  stimulated,  changes 
in  electric  potential  arise,  and  these  can  be  recorded  if  a  sufficiently 

1  Hirschfelder,  A.  D.,  "  Some  Variations  in  the  Form  of  the  VenoiTS  Pulse,"  Bull, 
of  the  Johns  Hopkins  Hosp.,  Baltimore,  1907,  xviii.,  265. 

2  Gibson,  A.  G.,  "The  Significance  of  a  hitherto  undescribed  Wave  in  the  Jugular 
Pulse,"  Lancet,  Lond.,  1907,  ii.,  1380. 


8  INTEODUCTION 

sensitive  galvanometer  be  used.  The  part  of  a  muscle  that  is  in  con- 
traction becomes  electro-negative  to  the  passive  parts,  and  thus  corre- 
sponds to  the  zinc  plate  of  a  galvanic  cell,  whereas  the  passive  parts 
correspond  to  the  copper  plate.  Waller,^  in  1887,  studied  the  action 
currents  of  the  human  heart  by  means  of  the  capillary  electrometer, 
and  he  showed  that  they  could  be  led  off  from  the  skin  surface;  but 
it  was  not  until  1903  that  Einthoven^  introduced  the  string  galvano- 
meter. It  is  this  instrument,  or  one  of  its  modifications,  that  is  now 
used  as  the  electrocardiograph  in  physiological  and  clinical  laboratories. 
The  instrument  consists  essentially  of  an  extremely  fine  fibre  of 


WWv  MW  v/w 


Fig.  8. — Control  curves  showing  that  the  deflexion  of  the 
fibre  becomes  increased  when  the  resistance  is 
lowered,  and  that  the  deflexion  time  is  increased 
when  the  tension  of  the  fibre  is  diminished.  In  each 
record  a  difference  of  potential  of  1  millivolt  was 
introduced  into  the  galvanometer  circuit.  In  a  and  c 
the  resistance  was  1500  ohms  greater  than  that  in  h. 
The  deflexion  time  in  a  is  0'017  second  ;  in  c  the 
tension  of  the  fibre  was  relaxed,  the  deflexion  is  of 
greater  amplitude,  and  the  deflexion  time  is  0'046 
second. 

silvered  glass  or  quartz,  suspended  between  the  poles  of  a  powerful 
electromagnet  and  at  right  angles  to  the  lines  of  force.  Each  end  of 
this  fibre  can  be  connected  to  a  non-polarisable  electrode  in  which  the 
patient  immerses  a  hand  or  foot.  The  action  currents  of  his  heart, 
being  thus  led  off  from  the  skin,  pass  through  the  fibre  which  becomes 
deflected  to  one  or  other  side  according  to  the  direction  of  the  current 
passing  through  it.  By  means  of  an  arc  lamp,  a  substage  condenser,  a 
microscope,  and  a  recording  apparatus,  the  shadow  of  the  moving  fibre 

1  Waller,  A.  D.,  "  A  Deinonstration  on  Man  of  Electromotive  Changes  accom- 
panying the  Heart's  Beat,"  Journ.  of  Physiol.^  Camb.,  1887,  viii.,  229. 

2  Einthoven,  W.,  "  Ein  neues  Galvanometer,"  Annalen  d.  Physik,  Leipz.,  1903, 
4  Eolge,  xii.,  1059  ;  "  Die  Koiistruktion  des  Saitengalvanometers,"  Arch.  f.  d.  ges. 
Physiol,  Bonn,  1909,  cxxx.,  287. 


THE   ELECTROCARDIOGRAM  9 

can  be  registered  on  a  photogiapliic  plate  or  tiliu.  The  record  thus 
obtained  is  an  electrocardiogram.  The  instrument  is  extremely 
sensitive,  aiul  if  the  fibre  be  properly  adjusted  it  is  absolutely  aperiodic 
and  has  a  detlexion  time  of  about  0"02  second. 

Tiie  amplitude  of  detlexion  of  the  fibre  is  proportionate  to  the 
strength  of  current  passing  through  it  and  to  that  of  the  magnetic 
field,  and  is  inversely  proportionate  to  the  weight  and  tension  of  the 
fibre  (Fig.  8).  The  strength  of  the  magnetic  field  and  the  weight 
of  the  fibre  are  constant.  The  tension  of  the  fibre  can  readily  be 
standardised.  For  example,  before  each  observation  is  made,  the 
tension  of  the  fibre  is  adjusted  so  that  when  the  patient,  or  a  resistance 
box  substituted  for  him,  is  in  the  galvanometer  circuit  a  difference  of 
potential  of  1  millivolt  gives  a  defiexion  of  1  cm.  This  standard,  intro- 
duced by  Einthoven,  is  generally  adopted  in  electrocardiographic  work. 


Q 


Fig.  9.—  Xormal  electrooardiogram  by  derivation  II.    The  time  record  is  2S"5~  per  second. 

The  form  of  the  electrocardiogram  differs  somewhat  in  any  one 
individual  according  as  the  electrodes  are  applied  to  one  or  other  part 
of  the  body  surface.  Following  Einthoven,^  we  speak  of  derivation  I. 
when  the  currents  are  led  off  from  the  right  hand  and  left  hand,  and 
of  derivations  II.  and  III.  when  the  right  hand  and  left  foot,  and  left 
hand  and  left  foot,  respectively  are  employed. 

A  normal  electrocardiogram  by  derivation  II.  is  shown  in  Fig.  9, 
whije  an  electrocardiogram  with  a  simultaneous  record  of  the  jugulo- 
carotid  pulsations  is  shown  in  Fig.  10.  The  normal  electrocardiographic 
deflexions  are  named  P,  Q,  E,  S,  and  T.  Each  upward  deflexion  signifies 
predominant  negativity  (activity)  at  the  base  or  right  side  of  the  heart ; 
each  downward  deflexion  indicates  predominant  negativity  (activity) 
at  the  apex  or  left  side  of  the  heart. 

Auricular  contraction  is  represented  by  the  deflexion  P,  which,  in 

1  Eintlaoven,  W.,  "Weiteres  iiber  das  Elektrokardiogramm,"  Arch.  f.  d.  ges. 
Physiol.,  Bonn,  1908,  cxxii.,  517. 


10  INTEODUCTION 

health,  is  monophasic  and  directed  upwards  (Fig.  11,  a).  In  some 
pathological  instances  the  auricular  deflexion,  although  monophasic,  is 
directed  downwards.  Again,  in  some  cases  of  auricular  flutter  and  in 
some  normal  hearts  under  vagus  inhibition  the  auricular  deflexion 
becomes  diphasic  (Fig.  11,  Ij).     These  abnormal  auricular  deflexions  are 


I    72.,  7J 


Fig.  10. — Jugulo-carotid  pulsations  and  electrocardiogram  by  derivation  II.    The  time  record  is  2S'57  per  second. 

generally  considered  as  evidence  of  the  auricular  contraction  having 
started  elsewhere  than  at  the  normal  site  (see  also  p.  93). 

During  the  interval  elapsing  between  the  end  of  P  and  the  com- 
mencement of  the  initial  ventricular  deflexion  {Q  or  R),  while  the  fibre 
is  at  rest,  the  stimulus  is  being  transmitted  along  the  atrio-ventricular 


a 

Fig.  11. — Diagrams  of  (a)  monophasic,  and  (6)  diphasic  deflexions. 

bundle  to  the  ventricles.  Q,  E,  S,  and  T  are  ventricular  deflexions. 
Although  their  precise  significance  is  still  undetermined,  we  know  that 
B,  which  is  the  most  constant  ventricular  deflexion,  precedes  the  apex- 
beat  and  the  first  sound  by  about  0-03  second  (Kahn,  Bull,  Fahr,  Lewis, 
Watson- Wemyss  and  Gunn^).     The  main  mass  of  ventricular  muscle 

1  Kahn,  R.  H.,  "  Die  Lage  der  Herztone  im  Elektrokardiogramme,"  ^rc/t./.  d.ges. 
Physiol.,  Bonn,  1910,  cxxxiii.,  .597  ;  Bull,  L.,  "  On  the  Simultaneous  Record  of 
the  Phono-  and  Electro-cardiogram,"  Quart.  Journ.  of  Exper.  Physiol.,  Lond.,  1911, 
iv.,    289 ;   Fahr,    G.,    "  On  Simultaneous  Records   of   the  Heart   Sounds  and   the 


THE   ELECTKOCARDIOGRAM 


11 


is  in  contraction  during  the  interval  S-T.  The  action  currents  probably 
compensate  one  another  meanwhile,  so  that  there  is  no  predominant 
activity  either  at  base  or  apex  or  in  right  or  left  ventricle.  In  the  case 
of  a  healthy  heart  the  terminal  detlexion  T,  as  recorded  by  derivation  I., 
is  directed  upwards,  and  probably  indicates  predominant  activity  of  the 
right  ventricle  over  the  left  at  the  end  of  systole.  In  many  cases  of 
lieart  failure,  T,  by  derivation  I.,  is  either  of  small  amplitude  or  is 
directed  downwards. 

The  particular  value  of  an  electrocardiogram  is  the  information  it 
yields  regarding  the  sequence  in  which  the  various  parts  of  the  cardiac 
muscle  pass  into  contraction.     Contractions  which  originate  at  abnormal 


X-J^ 


iunuiiimuuniiiiiiimAiimAJUiiiAAMmMii 

3 


Fig.  12. 


-Electrocardiograms.    1  and  2  are  by  derivation.s  I.  and  III.  from  a  ea.se  of  mitral  stenosis 
3  and  4  are  by  derivations  I.  and  III.  from  a  case  of  aortic  incompetence. 


sites,  or  w^hich  spread  through  the  heart  in  an  abnormal  manner, 
are  represented  by  electrocardiographic  deflexions  of  abnormal  form. 
Moreover,  the  form  of  the  ventricular  deflexions  may  show  departures 
from  the  normal  according  as  the  right  or  left  ventricle  is  in  pre- 
dominant  hypertrophy  (Eig.  12),  and  also  according  as  the  vagus  or  the 
sympathetic  fibres  to  the  heart  are  stimulated.  Not  the  least  important 
advantage  of  the  electrocardiograph  over  the  polygraph  is  the  ease 
wherewith  the  auricular  contractions  can  be  recorded  and  their  nature. 

Electrocardiogram,"  Heart,  Lond.,  1912-13,  iv.,  147;  Lewis,  T.,  "Tlie  Time 
Relations  of  Heart  Sounds  and  Murmurs,  with  Special  Reference  to  the 
Acoustic  Signs  in  Mitral  Stenosis,"  Heart,  Lond.,  1912-13,  iv.,  241  ;  Watson- 
Wemyss,  H.  L.,  and  Gunn,  J.  D.,  "  Simultaneous  Electro-  and  Phono-cardiograms,'' 
Edi?i.  Med.  Journ.,  Edin.,  1913  (X.  S.),  xi.,  124. 


12  INTEODUCTION 

whether  normal  or  abnormal,  can  be  demonstrated.  Electrocardiograms 
are  therefore  of  the  utmost  value  m  the  recognition  of  all  abnormal 
forms  of  auricular  contraction. 


EXTRASYSTOLES 

It  has  long  been  known  that  if  the  heart  be  excised  and  placed 
under  suitable  conditions  it  may  continue  to  beat  rhythmically  for 
hours.  The  site  at  which  the  stimuli  for  contraction  are  initiated  is 
therefore  within  the  heart  itself.  According  to  the  myogenic  theory, 
which  is  based  in  great  measure  on  the  epochal  researches  of  Gaskell,^ 
stimulus  production  and  the  conduction  of  stimuli  from  one  part  of  the 
heart  to  another  are  inherent  automatic  functions  of  the  heart  muscle. 
According  to  the  neurogenic  theory,  however,  the  stimuli  for  the 
heart's  contraction  are  generated  in,  and  conducted  by,  nerve  elements. 
Whichever  theory  be  correct,  rhythmic  stimuli  are  initiated  in  the 
healthy  heart,  the  muscle  fibres  receive  each  stimulus,  contract  in 
response  thereto,  and  maintain  a  certain  degree  of  tone.  The  function 
of  stimulus  production  is  most  highly  developed  in  the  sinus,  v^^hether 
it  be  the  sinus  venosus  itself,  or,  as  in  the  mammalian  heart,  the 
specialised  tissue  in  the  sinus  node  and  in  the  ostial  portions  of  the 
great  veins.  The  sinus  therefore  sets  the  pace  and  rhythm  of  the 
whole  heart.  In  health,  the  other  chambers,  being  endowed  with  a  less 
frequent  capacity  to  initiate  contractions,  beat  only  when  a  stimulus 
from  the  sinus  is  transmitted  to  each  of  them  in  sequence. 

Heart  muscle  differs  from  skeletal  muscle  in  two  fundamental 
respects.  If  a  stimulus  applied  to  the  heart  be  strong  enough  to  evoke 
a  contraction,  this  is  not  proportionate  to  the  strength  of  the  stimulus 
but  is  alv/ays  maximal.  This  phenomenon  constitutes  the  "all  or 
none  "  law  of  Bowditch.^  Again,  while  the  heart  muscle  is  in  contrac- 
tion it  is  incapable  of  excitation — the  heart  is  in  the  refractory  phase. 
During  diastole,  excitability  is  restored  gradually, 

A  response,  in  the  form  of  a  premature  beat  or  extrasystole,  is 
evoked  if  a  stimulus  of  effective  strength  is  applied  to  the  heart  muscle 
after  its  refractory  phase  has  ended,  and  yet  before  the  succeeding 
physiological  stimulus  is  due.     An  extrasystole  may  therefore  be  defined 

1  Gaskell,  W.  H.,  "  The  Contraction  of  Cardiac  Muscle,"  Schcifer's  Text-Book  of 
Physiology,  Edin.  and  Lond.,  1900,  ii.,  169-227. 

2  Bowditch,  H.  P.,  "  Ueber  die  Eigentliiimlichkeiten  der  Reizbarkeit,  welclie  die 
•  Muskelfasern  des  Herzens  zeigen,"  Ber.  uber  d.  Verhandl.  d.  Jconig.  sachs.  Gesell.  d.  TViss., 

Math.-phys.  Classe,  Leipz.,  1871,  xxiii.,  652. 


EXTEASYSTOLES 


13 


as  a  premature  beat  of  the  auricles  and  ventricles,  of  auricles  alone,  or 
of  ventricles  alone,  in  response  to  a  heterotopic  stimulus,  namely,  to 
one  that  is  initiated  at  some  part  of  the  heart  other  tliau  the  physio- 
logical pacemaker.  If  the  excitability  of  some  portion  of  the  heart  1)6 
unduly  high,  the  application  of  a  relatively  weak  stimulus  may  excite 


Fig.  13.— In  tlip  lower  (apical)  tracing  the  seventh  beat  is  an  extrasystole.  In  the  upper  (brachial) 
tracing  the  corresponding  pulse-wave  is  small  and  delayed.  From  a  man,  aged  (53,  with  aortic  and 
mitral  incompetence. 


Fig.  14. — An  extrasystole  followed  by  a  fully  compensatory  pause. 


Fig.  1').— Tlie  extrasystole  does  not  cause  a  pulse-wave,  but  the  post-extrasystolic  pause  is  fully  compensatory. 


Fig.  le. — The  extrasystole  is  followed  by  a  pause  that  is  not  fully  compensatory. 


an  extrasystole,  whereas   in   the   case   of    a  healthy  heart  a  stronger 
stimulus  would  be  necessary. 

The  most  obvious  and  constant  character  of  an  extrasystole  is  its 
premature  incidence  in  the  course  of  a  series  of  rhythmic  physiological 
beats.  In  some  extrasystoles  only  the  ventricles  contract  prematurely, 
the  auricles  meanwhile  pursuing  an  unchanged  rhythm,  but  in  other 
instances  both  the  auricles  and  ventricles  contract  prematurely.  In 
either  case  the  premature  beat  of  the  ventricles  may  open  the  semi- 


14  IXTEODUCTIOX 

lunar  valves  and  thus  transmit  a  pulse-wave  into  the  arteries,  or  may- 
fail  to  do  so  (Figs.  14,  15). 

As  was  pointed  out  by  Marey,^  an  extrasystole  is  usually  followed 
by  a  diastolic  pause — a  post-extrasystolic  pause — of  longer  duration  than 
that  after  each  physiological  beat.  In  many  instances  the  rhythm  of 
the  sinus  is  not  disturbed  by  the  extrasystole,  and  the  post-extrasystolic 
pause  is  then  exactly  compensatory  (Fig.  14).  The  subsequent  ven- 
tricular beats  therefore  occur  at  precisely  the  same  time  as  if  there  had 
been  no  extrasystole.  In  other  instances,  when  the  stimulus  that 
excites  the  extrasystole  travels  back  to  the  sinus  and  disturbs  its 
rhythm,  the  post-extrasystolic  pause  is  not  fully  compensatory  (Fig.  16). 
In  rare  instances  the  pause  after  an  extrasystole  may  even  be  shorter 
than  that  after  each  physiological  beat,  and  if  the  post-extrasystolic 
pause  is  so  short  that  the  following  beat  is  not  retarded  at  all,  the 
extrasystole  is  said  to  be  interpolated  (Plate  Y.,  Fig.  18). 

Varieties  of  Extr asystoles. — Extrasystoles  may  start  in  any  portion 
of  the  heart.  Those  that  are  held  to  originate  in  the  remains  of  the 
sinus  (sinus  extrasystoles),  in  the  auricles  (auricular  extrasystoles),  and 
in  the  atrio-ventricular  node  and  bundle  (nodal  extrasystoles)  may  be 
grouped  together  as  supra-ventricular  extrasystoles.  A^entricular  extra- 
systoles originate  either  in  the  ventricular  muscle  or  in  the  branches  of 
the  atrio-ventricular  bundle.  The  characters  that  differentiate  supra- 
ventricular from  ventricular  extrasystoles  are  well  defined  and 
distinctive,  but  the  differentiation  of  one  variety  of  supra-ventricular 
extrasystole  from  another  is  more  speculative. 

A  ventricular  extrasystole  can  be  recognised  readily.  The  apical 
impulse  is  premature,  and  if  the  aortic  valve  be  opened  and  a  pulse- 
wave  transmitted  into  the  arteries,  this  pulse-wave  is  also  premature 
(Fig.  13).  The  auricular  rhythm  is  not  disturbed  (Fig.  17).  The 
premature  beat  of  the  ventricles  is  usually  coincident  with  a  rhythmic 
auricular  beat,  and  as  the  auriculo-ventricular  valves  are  meanwhile 
closed  and  the  auricles  are  therefore  unable  to  drive  onwards  their  con- 
tained blood,  they  propel  it  backwards  into  the  great  veins,  and  thus 
a  large  wave  appears  in  the  jugular  veins.  The  post-extrasystolic  pause 
is,  as  a  rule,  fully  compensatory. 

As  contrasted  with  the  electrocardiographic  deflections  Q,  B,  S, 
and  :Z'  of  a  physiological  beat,  a  ventricular  extrasystole  is  represented 
by  an  "atypical  deflexion"  which  is  usually  of  diphasic  form  (Fig.  17). 

1  Marey,  E.  J.,  Physiologie  exjyerivientale,  Travauz  du  Laboratoire  cle,  Paris,  1876, 
ii.,  63-86. 


I'l.ATK    IV. 


X 

t 
t 
t 
t 

t 

\ 

t 
t 

t 
t 


t 
1 


.2      o 


O     Q 


C       53  O 


■r  G 


V.S 


S  II  £  'I 


V)  =1^ 


PLATE  V. 


Fig.  is. — Sphygmogram  and  electrocardiogram  by  derivation  II.,  showing  an 
interpolated  extrasystole.  The  inter-ventricular  periods  of  the  physiological 
beats  are  successively  O'SO,  0'84,  0'84  second. 


aiUUHHUUHIUIIIUUiUHUULU 


6. 


Fig.  19. — Electrocardiograms;  a,  Derivation  I.  ;  b,  Derivation  III.  Both  show 
a  normal  beat  and  an  extrasystole  of  type  1.  Prom  a  man,  aged  45,  with 
aortic  incompetence  and  heart  failure,  who  died  a  fortnight  later.  1  cm. 
=  1  millivolt. 


mmiimmimmiimammti    iHiyiJliiiitlUltiliiitttllliJiitiiliiiitiiiiiiiiiiiii 


a.  T). 

Pig.  20. — Electrocardiograms  ;  a,  Derivation  I.  ;  6,  Derivation  III.  In  botli 
records  the  second  beat  is  an  extrasystole  of  type  2.  Prom  a  man,  aged 
69,  with  calcareous  arteries,  a  systolic  blood-pressure  of  285  mm.  Hg, 
dropsy,  albuminuria,  and  auricular  fibrillation.     1  cm.  =1  millivolt. 


EXTRASYSTOLES  15 

This  indicates  that  the  various  parts  of  the  ventricular  musculature  are 
not  passing  into  activity  in  normal  se(iuence.  The  form  of  the  dellexiou 
varies  according  to  the  site  of  initial  stimulation,  whether  on  the  right 
or  left  side,  for  example,  and  according  to  the  derivation  employed  in 
recording  the  electrocardiogram.  If  the  action  currents  are  led  off 
from  the  patient's  left  hand  and  left  foot  (derivation  III.)  the  initial 
deflexion  may  be  downwards  and  the  terminal  deflexion  upwards 
(Fig.  19,  b).  In  this  case  the  extrasystole  is  held  to  arise  in  the  apex 
or  left  ventricle,  and  possibly  in  the  terminal  fibres  of  the  left  branch 
of  the  atrio-veiitricular  bundle.  If,  with  the  same  derivation  (deriva- 
tion III.),  the  initial  deflexion  is  upwards  and  the  terminal  deflexion  is 
downwards  (Fig.  20,  h),  the  extrasystole  is  regarded  as  arising  in  the 
base  or  right  ventricle,  and  possibly  in  the  terminal  fibres  of  the  right 
branch  of  the  bundle.  If,  however,  the  records  were  taken  by  deriva- 
tion I.  (right  hand  and  left  hand),  the  form  of  the  deflexions  is  usually 
the  reverse  of  that  by  derivation  III.  Thus  a  left  apical  extrasystole 
by  derivation  I.  yields  a  curve  similar  to  that  of  a  right  basal  extra- 
systole by  derivation  III.  (Figs.  19,  a,  and  20,  h).  The  former  is  the 
more  common. 

In  a  supra-ventricular  extrasystole  both  auricles  and  ventricles 
contract  prematurely,  and  as  the  rhythm  of  the  sinus  is  disturbed  the 
post-extrasystolic  pause  is  not  fully  compensatory.  If  the  auricles 
begin  to  contract  before  the  ventricles  (Fig.  21),  the  extrasystole 
probably  originates  either  in  the  vicinity  of  the  sinus  node  or  in  the 
auricular  muscle.  In  the  former  case  the  auricular  deflexion  is  of 
normal  form.  In  many  instances,  however,  the  form  of  the  auricular 
deflexion  is  abnormal,  and  it  is  often  inverted,  indicating  that  the 
auricular  contraction  began  elsewhere  than  at  the  normal  site.  The 
ventricular  beat  usually  yields  a  perfectly  normal  electrocardiogram, 
because  the  stimulus  passes  to  the  ventricles  by  means  of  the  normal 
pathway,  the  atrio-ventricular  conducting  system. 

In  a  "nodal"  extrasystole'^  the  auricles  and  ventricles  contract 
prematurely  and  simultaneously.  In  some  nodal  extrasystoles  the 
ventricles  begin  to  contract  before  the  auricles,  but  in  others  the 
auricles  begin  to  contract  about  0"06  second,  or  less,  before  the  ventricles. 
But  even  in  the  latter  instances,  with  an  As—  Vs  interval  shorter  than 
normal  (0*14  second)  the  auricles  are  still  in  systole  when  the  ventricles 

^  Mackenzie,  J.,  "The  Extra-systole:  A  Contribution  to  the  Functional 
Pathology  of  the  Primitive  Cardiac  Tissue,"  Quart.  Journ.  of  Med.,  Oxford,  1907-8, 
i.,  131,  481. 


16  INTRODUCTION 

begin  to  contract,  because  auricular  systole  lasts  about  0*1  second. 
Whether  the  ventricles  or  the  auricles  begin  to  contract  first,  the  fact 
of  their  being  in  contraction  simultaneously  suggests  that  the  stimulus 
for  their  contraction  is  generated  at  a  site  more  or  less  midway  between 
them,  and  probably  at  the  atrio-ventricular  node  or  bundle  (see 
also  p.  115). 

As  a  rule  extrasystoles  occur  singly,  but  there  may  be  multiple 
ex trasy stoles,  one  after  another.  Again,  in  any  one  patient  all  the 
extrasystoles  are  usually  of  one  and  the  same  variety,  yield  the  same 
form  of  electrocardiogram,  and  presumably  originate  at  the  same  site 
in  the  heart  wall. 

Although  extrasystoles  undoubtedly  indicate  an  irritable  focus  in 
the  heart,  their  clinical  significance  has  been  the  subject  of  much  con- 
troversy. Some  authorities  regard  them  as  of  little  moment ;  others 
maintain  that  they  indicate  a  definite,  even  though  slight,  impairment 
of  the  heart's  functional  efficiency.  In  my  own  experience,  extrasystoles 
may  be  of  purely  nervous  origin,  but  as  a  rule  they  have  been  associated 
with  some  insufficiency  of  the  heart  muscle.  The  defect  may  be  slight 
and  transient,  as  in  the  course  of  an  acute  infective  disease.  More  often 
extrasystoles  are  either  an  early  indication  of  arterio-sclerosis  in  an 
apparently  healthy  heart,  or  are  associated  with  signs  of  more  or  less 
obvious  heart  failure,  such  as  dyspnoea  on  exertion,  precordial  pain,  and 
dropsy.  In  about  30  per  cent,  of  my  cases  the  larger  arteries  of  the 
arm  were  notably  thickened,  and  about  the  same  percentage  of  cases 
presented  evidence  of  mitral  disease.  Combined  mitral  and  aortic 
lesions  were  found  in  16  per  cent. 

From  an  analysis  of  32  cases  with  supra- ventricular  extrasystoles  it 
appears  that  the  prognosis  in  such  cases  is  particularly  unfavourable. 
Of  these  32  cases,  7  subsequently  developed  persistent  auricular  fibrilla- 
tion, and  at  least  10  of  the  32  cases  are  known  to  have  died  within 
about  two  years  after  the  extrasystoles  were  recorded.  In  some  of  these 
cases  the  fatal  issue  ensued  in  the  course  of  a  few  weeks.  For  example, 
in  a  mason  aged  49,  a  big,  sturdily-built  man,  who  had  been  subject  to 
nocturnal  attacks  of  precordial  pain  for  two  years,  numerous  auricular 
extrasystoles  were  recorded  (Fig.  21).  The  patient  was  not  dropsical, 
nor  indeed  was  he  so  ill  as  to  necessitate  his  being  confined  to  bed. 
Two  days  after  the  last  electrocardiogram,  showing  auricular  extra- 
systoles, was  recorded,  he  died  suddenly.  The  post-mortem  examination 
revealed  chronic  mediastino-pericarditis  with  chronic  venous  congestion 
of  the  liver,  spleen  and  lungs,  and  in  the  lungs  there  was  also  much 


ri,A'i'i':  \i. 


'^f^^^l'^l^^^^j^^ 


Fiii.  21. — Electiocar(iio,u;iani  by  derivation  II.  Tin-  tliiicl  and  sixth  beats  are  auricular  extrasystoles.  In  llie 
l'orn\er  the  auricular  deflexion  is  uieryed  with  the  terminal  ventricular  deflexion  of  the  antecedent  heat. 
From  a  case  of  syphilitic  aortitis  and  myocarditis,  three  days  before  death. 


/     J^lil 


Fig.  22. — Syphilitic  aortitis. 


AURICULAR   FIBRILLATION  17 

fibrous  iiuluratioii  as  a  result  of  silicosis.  All  tlie  chambers  of  the  heart 
were  dilated,  and  all  except  the  left  ventricle  were  hypertrophied.  The 
orifice  of  the  left  coronary  artery  was  almost  occluded  by  extensive 
sypliilitic  infiltration  and  scarring  in  the  wall  of  the  aorta  (Fig.  22), 
and  there  were  many  fibrous  patches  in  the  wall  of  the  left  ventricle. 
The  right  auricle  revealed  only  a  slight  degree  of  fibrosis  without  any 
leucocytic  infiltration,  while  the  atrio-ventricular  node  and  bundle  were 
healthy. 

In  this  case  the  auricular  extrasystoles  were  probably  followed  by 
auricular  fibrillation,  and  the  patient's  sudden  death  may  have  been 
due  to  the  ventricles  subsequently  passing  into  fibrillation  in  the 
manner  suggested  first  by  Mac  William^  and  afterwards  by  Hering- 
and  others.  In  this  case,  and  in  others  where  supra-ventricular  extra- 
systoles  were  know^n  to  be  the  precursors  of  auricular  fibrillation,  with 
or  without  an  intermediate  stage  of  auricular  fiutter,  the  sequence  of 
events  suggests  that  the  pathological  changes  in  the  walls  of  the  auricles 
became  progressively  more  intense  and  diffuse. 


AuiilCULAE    FlBKILLATIOX 

When  the  co-ordinate  contraction  of  the  auricular  musculature 
becomes  replaced  by  inco-ordinate  fibrillar  contraction,  the  auricles 
dilate  and  are  rendered  functionally  inactive  in  so  far  as  they  fail 
to  expel  their  contained  blood  into  the  ventricles.  Each  ventricular 
contraction  is  still  a  co-ordinate  one,  but,  as  was  shown  experiment- 
ally by  MacWilliam,^  Philips,^  and  Fredericq,*  the  ventricular  rhythm 
becomes  wholly  disorderly,  and  the  rate  of  ventricular  contraction  is 
usually  much  accelerated.  The  suggestion  made  by  Cushny  and 
Edmunds''  that  complete  irregularity  of  the  ventricles  in  man  might 
be  due  to  auricular  fibrillation  was  proved  to  be  correct  by  liothberger 

1  MacWilliam,  J.  A.,  "  Fibrillar  Contraction  of  the  Heart,"  Journ.  of  Physiol., 
€amb.,  1887,  viii.,  296. 

2  Hering,  H.  E.,  "  Ueber  plotzlichen  Tod  durcli  Herzkammerflimniern,"  MUnch. 
tned.  Wochmckr.,  1912,  lix.,  750,  818. 

'  Philips,  F.,  "  Les  tremulations  tibrillaires  des  oreillettes  et  des  ventricules  dii 
ca'ur  du  chien,"  Arch,  internat.  de x^hyaiol .,  1904-5,  ii.,  271. 

*  Fredericq,  L.,  "  Rhythme  aftble  des  ventricules  du  ti  la  fibrillation  des  oreillettes. 
Physiologie  du  faisceau  auriculo-ventriculaire,"  ibid.,  1904-5,  ii.,  281. 

5  Cushny,  A.  R.,  and  Edmunds,  C.  W.,  "  Paroxysmal  Irregularity  of  the  Heart 
and  Auricular  Fibrillation,"  Studies  in  Pathology,  edited  by  Bulloch,  Aberdeen,  1906, 
95  ;  Aniei:  Journ.  Med.  Sci.,  Philad.,  1907,  cxxxiii.,  66. 

9 


18 


INTRODUCTION" 


and  Winterberg^  in  1909,  and  subsequently  by  the  independent  work 
of  Lewis  ^  and  Jolly  and  myself.^ 

In  the  human  heart  auricular  fibrillation  is  one  of  the  most  frequent 
forms  of  irregularity.  It  is  decidedly  more  frequent  in  patients  over 
forty  years  of  age  than  in  younger  individuals.  Males  are  twice  as 
frequently  affected  as  females,  and  in  about  one-half  of  the  cases  there 
is  evidence  of  arterio-sclerosis.  Fibrillation  is  especially  common  in 
cases  of  chronic  interstitial  myocarditis  and  in  the  terminal  stages  of 
mitral  disease. 

Auricular  fibrillation   may  take   the   form  of  paroxysmal  attacks 


®, 


Fig.  23. — NoRiiAL  Heart,  Female  Patient,  aged  32. 

1.  In  deep  expiration.    2.  In  tranquil  inspiration.    3.  In  deep  inspiration. 

A,  Curve  of  aorta.  P,  Pulmonary  curve.  LA,  Left  auricular  curve. 
V,  Left  ventricular  curve.  SC,  Curve  of  superior  vena.  cava. 
JRA,  Curve  of  right  auricle.  The  position  of  the  episternal 
notch,  level  of  third  chondro-sternal  articulation,  the  nipples  and 
umbilicus  shown.    X  indicates  the  position  of  the  apex-beat. 

during  which  the  ventricular  rate  may  rise  to  120-150,  and  in  some 
cases  even  to  180-190  per  minute.  The  initial  attacks  begin  and 
end  abruptly,  but  sooner  or  later  fibrillation  becomes  persistent.  The 
paroxysmal  form  was  observed  in  a  young  woman  aged  22,  who  was 
affected  with  mitral  stenosis.  When  she  was  admitted  to  hospital,  her 
pulse   had  a  rate  of  160-162  per  minute.     On  the  following  morning 

1  Eothberger,  J.,  and  Winterberg,  H.,  "  Vorhofflimmern  uiid  Arhythmia  per- 
petua,"  Wie7i.  Jclin.  Wochenschr.,  1909,  xxii.,  839  ;  "  Ueber  das  Elektrokardiogramm 
bei  Flimmern  der  Vorhofe,"  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1910,  cxxxi.,  387. 

2  Lewis,  T.,  "  Auricular  Fibrillation  and  its  Kelation.sliip  to  Clinical  Irregularity 
of  the  Heart,"  Heart,  Lond.,  1909-10,  i.,  306. 

3  Jolly,  W.  A.,  and  Ritcbie,  W.  T.,  "Auricular  Flutter  and  Fibrillation,"^£'ear^,. 
Lond.,  1910-11,  ii.,  177. 


AURIC ULAli   FTUrJLT.A'riOX 


19 


the  noinial  iliytlnu  was  restored,  and  the  rate  was  then  77  per  minute. 
Fifteen  months  later  this  rhythm  was  still  maintained. 

A  second  example  of  paroxysmal  tibrillation  was  that  of  an  old 
gentleman  who  had  enjoyed  excellent  health  ever  since  childhood. 
At  the  age  of  73,  however,  he  had  thickened  arteries  and  an  aortic 
systolic  murmur.  As  a  rule  the  rate  of  his  pulse  was  about  78  per 
minute  and  its  rhythm  was  perfectly  regular  except  for  an  occasional 
extrasystole.  His  paroxysmal  attacks  of  auricular  fibrillation  came  on 
by  day  or  by  night,  and  usually  lasted  for  several  hours.  Sometimes 
after  having  retired  to  bed  feeling  perfectly  well,  and  having  slept 
soundly  for  several  hours,  he  would  awake  feeling  weak  and  ill,  and 


Fig.  24. — Mitral  Stenosis,  with  Auricular  Fibrillation, 
Female,  aged  25. 

A  large  globular  heart. 

The  deep  percussion  dulness  of  the  heart. 

X  X  X  X  X  X  The  superficial  percussion  dulness. . 

his  pulse  would  then  be  extremely  irregular  and  its  rate  about  160-170 
per  minute. 

A  third,  and  still  more  striking,  case  of  paroxysmal  fibrillation  was 
that  of  a  man  aged  46,  who  had  been  ailing  for  a  year  and  who,  six 
months  before  I  saw  him,  had  been  seized  suddenly  with  what  he  called 
"  a  fluttering  at  the  heart,"  accompanied  by  a  violent  paroxysm  of  cough- 
ing. He  was  an  emaciated,  anxious-looking  man,  whose  clothes  hung 
loosely  on  him,  for  he  had  lost  5  stones  in  weight.  His  heart  was  not 
enlarged  and  both  sounds  were  pure,  but  as  ascertained  by  means  of 
the  screen  the  aortic  arch  was  dilated.  When  the  cardiac  rhythm  was 
normal  at  the  rate  of  about  100  per  minute,  he  was  liable  to  severe 
attacks  of  pain  in  the  precordial  region  and  left  arm.  Morphia  alone 
afforded  him  relief.     From  time  to  time  he  suffered  from  sudden  attacks 


20 


INTEODUCTION 


of  auricular  fibrillation,  with  a  ventricular  venous  pulse  and  complete 
arrhythmia  of  the  ventricles  at  a  rate  of  about  120  per  minute. 
During  these  attacks  he  felt  the  "  fluttering,"  but  never  any  pain. 
The  attacks  used  to  pass  off  spontaneously  and  suddenly,  and  they 
sometimes  ceased  while  he  was  asleep. 

He  had  been  taking  strophanthus  for  several  months  without 
obtaining  real  benefit.  But  within  a  fortnight  of  his  commencing  to 
take  potassium  iodide  he  was  free  of  both  the  pain  and  the  paroxysmal 
attacks  of  fibrillation,  and  was  able  to  eat  heartily  and  sleep  soundly. 
His  health  was  soon  so  far  restored  that  he  was  able  to  travel  to  the 


Fig.  25. — Auricular  Fibrillation,  Male,  aged  21. 

The  deep  percussion  dulness. 

X   X   X  X   X   X  The  superficial  percussion  dulness  in  full  expiration. 
—  .  —  .  -—  .  —  The  supertleial  percussion  dulness  in  full  inspiration. 

south  of  England  in  search  of  sunshine  and  warmth.     Two  months  later 
he  died  suddenly. 

In  a  large  number  of  cases,  auricular  fibrillation  passes  from  the 
paroxysmal  into  the  persistent  form.  The  heart  often  becomes  dilated 
and  its  outline  more  or  less  globular  (Figs.  24  and  25).  The  transverse 
diameter  of  the  heart  becomes  notably  increased.  In  ten  consecu- 
tive cases  of  fibrillation  studied  by  means  of  orthoradiography,  Hope 
Eowler  ^  and  the  writer  found  the  average  maximum  transverse  diameter 
to  be  15 "4  cm.,  while  the  average  long  diameter,  from  the  cavo-auricular 
junction  to'the  apex,  was  16*4  cm.     In  healthy  adult  males  the  average 


^  Fowler,  W.  Hope,  and^Ritchie,  W.  T.,  "  Orthoradiography  of  the  Heart  and 
Aorta,"  Edin.  Med.  Journ.,  Edin.,  1912  (N.  S.),  ix.,  197. 


AURICULAR   FIBRILLATION 


21 


transverse  and  long  diameters  of  the  heart  are  about  12-1-13  cm.,  and 
18-14  cm.  respectively. 

When  the  auricles  are  in  tibrillation  the  efficiency  of  the  heart  as  a 
pump  becomes  impaired  and  many  of  the  classic  symptoms  and  signs 
of  heart  failure  usually  supervene.  As  a  rule,  the  intensity  of  the 
symptoms  is  proportionate  to  the  rapidity  of  the  ventricular  rate. 
When  this  becomes  retarded,  as  by  means  of  digitalis,  the  urgent 
symptoms  often  vanish. 

The  jugular  imhc  in  auricular  fibrillation  acquires  the  ventricular 
form.     This  is   cliaracterised  by  the   absence    of   the   auricular   wave 


Fio.  2(3. — Auricular  fibrillation.    The  jugular  pulse  is  of  tlie  ventricular  form,  and  during  diastole 
small  irregular  wavelets  are  superposed  on  the  curve.    {Heart,  vol.  ii.) 


immediately  before  each  ventricular  systole  commences.  The  tracing 
rises  abruptly  with  the  onset  of  ventricular  systole,  and  the  systolic 
plateau,  which  may  be  interrupted  by  a  depression  due  to  the  systolic 
pull  of  the  papillary  muscles,  is  maintained  until  the  tricuspid  valve 
opens.  When  this  event  occurs,  and  the  blood  pent  up  in  the  auricles 
rushes  into  the  ventricles,  the  curve  falls  abruptly.  Thereafter,  it 
again  ascends  gradually  while  the  pressure  in  the  auricles  and  ventricles 
is  rising  during  ventricular  diastole.  During  this  latter  phase,  small 
irregular  wavelets  of  auricular  origin  may  be  superposed  on  the  line  of 
ascent  (see  Fig.  26). 

Electrocardiograms  do  not  present  a  normal  auricular  deflexion,  P; 
but  a  series  of  small  irregular  deflexions  at  a  rate  of  about  380  to  520 
per  minute  is   observed   during   ventricular  diastole  when   the   fibre 


22  INTEODUCTION" 

should  be  at  rest  (Fig.  27).  These  deflexions  are  most  evident  when 
the  electrocardiogram  is  recorded  by  derivation  III.  (left  hand  and  left 
foot).  Although  the  ventricular  rhythm  is  wholly  disorderly,  the 
ventricular  deflexions  are  essentially  of  normal  form,  which  indicates 
that  these  chambers  are  beating  in  response  to  stimuli  of  supra- 
ventricular origin. 

Auricular  fibrillation  may  be  regarded  as  the  combined  result  of 
two  functional  changes  in  the  auricular  muscle,  namely,  increased 
excitability  and  defective  conductivity.  It  is  not  always  possible  to 
correlate  these  changes  with  structural  alterations  in  the  auricular 
muscle,  yet  inflammatory  changes  are  usually  found.  Eadasewsky^ 
pointed  out  that  persistent  arrhythmia  of  the  ventricles  depends  mainly 
upon  diffuse  interstitial  myocarditis,  affecting  especially  the  right 
auricle.  Sub-acute  and  chronic  inflammation  of  the  structures  at  the 
superior  cavo-auricular  junction  has  been  described  by  Schonberg-  and 


[mail 


Fig.  27.— Auricular  fibrillation  with  an  infrequent  ventricular  rate.     Derivation  III. 
1'5  cm.=l  millivolt. 

Hedinger,^  while  Koch,*  Draper,^  and  others  have  recorded  fibrosis  of 
the  sinus  node.  Six  of  my  own  cases  presented  diffuse  fibrosis  and 
extensive  lymphocytic  infiltration  throughout  the  auricular  walls,  with 
similar  lesions  in  the  sinus  node  and  in  the  atrio-ventricular  conducting 
system.  These  structural  changes,  however,  are  not  uniformly  well 
marked. 

Experimental  observations  indicate   that   extrasystoles,   flutter,   or 

1  Radasewsky,  M.,  "Ueber  die  Muskelerkrankungen  der  Vorhofe  des  Herzens," 
Zeitschr.f.  Uin.  Med,  Berlin,  1895,  xxvii.,  ,381. 

2  Schonberg,  S.,  "Ueber  Veranderungeii  im  Siniisgebiet  des  Herzens  bei 
chronischer  Arrhytbmie,"  FranJcf.  Zeitschr.  f.  PatJwl,  Wiesbaden,  1 909,  ii.,  153; 
"Weitere  Untersucliungen  des  Herzens  bei  chronischer  Arrhythmie,"  ibid.,  1909, 
ii.,  462. 

2  Hedinger,  E.,  "Uber  Herzbefunde  bei  Arrhythmia  perpetua,"  ibid.,  1910, 
v.,  296. 

*  Koch,  W.,  "  Zur  pathologischen  Anatoniie  der  Rhythmusstorungen  des  Herzens," 
Berl.  hlin.  Wockenschr.,  1910,  xlvii.,  1108. 

^  Draper,  G.,  "Pulsus  irregularis  perpetuus -with  Fibrosis  of  the  Sinus  Node," 
Eeart,  Lond.,  1911-12,  iii.,  13. 


AUPJCULAIi  niUilLLATIOX  23 

fibrillation  can  be  induced  according  to  the  strength  of  stimulation 
applied  to  the  auricular  muscle ;  and  clinical  evidence  demonstrates 
that  auricular  flutter  may  be  preceded  by  supra-ventricular  extra- 
systoles  and  followed  by  fibrillation.  These  three  forms  of  abnormal 
auricular  action  may  therefore  be  regarded  as  representing  successive 
stages  of  abnormal  stimulation  of  the  auricles.  When  occasional  supra- 
ventricular extrasystoles  occur,  it  may  be  assumed  that  a  single 
abnormal  stimulus  of  effective  strength  is  being  generated,  from  time 
to  time,  at  an  irritable  focus  in  the  auricular  walls.  AVhen  multiple 
extrasystoles  occur,  the  stimuli  are  probably  being  generated  in  rapid 
succession.  AVhen  the  auricles  are  in  flutter,  the  abnormal  stimulation 
of  one  focus  in  the  auricular  musculature  is  probably  still  more  frequent 
and  intense,  leading  to  rhythmic  co-ordinate  contractions  of  the  auricles 
at  a  rate  that  is  greatly  accelerated.  Lastly,  auricular  fibrillation 
ensues  when  there  is  abnormal  stimulation  of  great  frequency  and 
intensity  at  many  foci,  and  when  there  is  defective  conduction  of 
stimuli  through  the  auricular  walls. 


CHAPTER  II 

ETIOLOGY 

AUEICULAE  flutter  is  a  pathological  action  of  the  auricles  characterised 
by  rhythmic  co-ordinate  contractions  of  their  musculature  at  a  rate 
that  is  greatly  accelerated,  and  is  usually  between  250  and  300  per 
minute.  The  term  "  auricular  flutter,"  as  applied  to  the  human  auricles, 
was  originally  employed  by  Jolly  and  myself^  in  1911.  The  condition 
has  also  been  described  under  the  designations  "jugular  embryo- 
cardia "  (Morison),^  "  auricular  tachysystole "  (Eihl),^  "  auricular 
tachycardia  "  (Robinson),"^  and  "  auricular  tachyrhythmia  "  (Hoffmann).^ 

In  the  preceding  chapter  it  has  been  mentioned  that  an  auricular 
extrasystole  is  induced  when  an  efl'ective  stimulus  is  applied  to  the 
auricular  muscle  after  its  refractory  phase  has  terminated,  but  before 
the  next  physiological  beat  is  due.  It  has  also  been  shown  that  when 
strong  faradic  stimulation  is  applied  to  the  auricles,  their  co-ordinate 
contraction  becomes  replaced  by  fibrillation. 

Auricular  flutter,  as  a  result  of  weak  faradisation  of  the  mammalian 
auricles,  was  first  described  by  Mac  William*'  in  1887.  He  stated  that 
"  the  application  of  the  current  sets  the  auricles  into  a  rapid  flutter,  the 
rapidity  of  which  largely  depends  upon  the  excitability  of  the  auricular 
tissue  and  the  strength  of  current  employed.  The  movements  are 
regular;  they  seem  to  consist  in  a  series  of  contractions  originating 
in  the  stimulated  area,  and  thence  spreading  over  the  rest  of  the 
tissue.      The   movement   does   not   show   any   distinct  sign    of    inco- 

1  Jolly,  W.  A.,  and  Ritchie,  W.  T.,  "Auricular  Flutter  and  Fibrillation,"  Heart, 
Lond.,  1910-11,  ii.,  177. 

2  Morison,  A.,  "Cardiac  Motion  as  Revealed  by  the  Vivisection  of  Disease," 
Lancet,  Lend.,  1909,  i.,  77  ;  ibid.,  1909,  i.,  39. 

^  Rihl,  J.,  "  Hochgradige  Vorhoftachysystolien  niit  Ueberleitmigsstorungen  und 
electiver  Vaguswirkung,"  Zeitschr.  f.  exper.  Pathol,  u.  Therwp.,  Berlin,  1911,  ix., 
277. 

•*  Robinson,  G.  Canby,  "The  Influence  of  the  Vagus  Nerves  on  the  Faradized 
Auricles  in  the  Dog's  Heart,"  Journ.  of  Exper.  Med.,  New  York,  1913,  xvii.,  429. 

5  Hoffmann,  A.,  Die  Elehtrographie  als  Untersucliiingsmethode  des  Herzens  und 
Hire  Ergebnisse,  Wiesbaden,  1914,  188-202. 

6  MacWilliani,  J.  A.,  "Fibrillar  Contraction  of  the  Heart,"  Journ.  of  Physiol., 
Camb.,  1887,  viii.,  296. 


EXPERIMENTAL  FLUTTEII  25 

ordination ;  it   looks  like  a  rapid  series  of  contraction  waves  passing 
over  tlie  auricular  walls." 

In  a  later  paper  (1888)  MacWilliam^  stated  that  when  faradic 
stimulation  of  moderate  strength  is  applied  to  the  right  or  left  auricular 
appendix  "the  auricles  are  thrown  into  a  state  of  rapid  fluttering 
action ;  and  this  movement  continues  during  the  passage  of  the  exciting 
current  and  for  a  considerable  time  afterwards — the  after-duration 
varying  according  to  the  excitability  of  the  auricular  tissue  and  the 
strength  of  the  current  employed.  The  individual  contractions  con- 
stituting the  rapid  fluttering  auricular  movement  are  weak  and  slight, 
as  might  be  expected.  Meanwhile  the  ventricles  beat  rapidly ;  much 
more  rapidly  than  usual,  though  their  action  is  not  nearly  so  rapid  as 
is  that  of  the  auricles.  The  ventricular  acceleration  appears  to  be  due 
to  the  propagation  of  a  more  rapid  series  of  beats  from  the  auricles. 
All  the  auricular  contractions  indeed  are  not  transmitted  to  the 
ventricles ;  often  not  more  than  one-half  or  even  less  are  transmitted, 
but  even  such  a  proportion  is  sufficient  to  cause  a  very  marked  accelera- 
tion in  the  ventricular  rate  of  beat.  It  is  very  possible  that  the  weak- 
ness of  the  rapidly-recurring  auricular  contractions  is  an  important 
factor  in  preventing  a  more  complete  propagation  to  the  ventricles. 
The  degree  of  acceleration  that  occurs  varies  considerably.  In  hearts 
beating  at  140-180  per  minute,  stimulation  of  the  auricular  appendix 
often  causes  the  auricular  rate  to  rise  as  high  as  500-600  per  minute ; 
meanwhile  the  ventricular  rhythm  may  have  a  rapidity  of  from  200-300 
per  minute  or  even  higher." 

The  clinical  disorder  that  is  designated  auricular  flutter  is  identical 
in  all  its  essential  features  with  the  flutter  induced  experimentally  by 
MacWilliam. 

MacWilliam  proceeded  to  describe  the  auricular  flutter  and  ven- 
tricular responses  upon  stimulation  of  the  "  inhibitory  area "  of  the 
mammalian  heart.  This  area  was  described  as  a  narrow,  elongated 
area  on  the  dorsal  aspect  of  the  auricles,  overlying  the  lower  part  of 
the  inter-auricular  septum  and  its  long  axis  running  parallel  with  the 
plane  of  the  latter.  When  this  area  of  the  auricular  wall  was  stimu- 
lated, "  the  auricles  are  thrown  into  rapid  fluttering  movement  much 
resembling  that  obtained  by  excitation  of  other  parts  of  the  auricular 
surface.  At  the  same  time  the  ventricles  stand  still  in  diastole  and  fill 
up  with  blood.      This  lasts   for  a  considerable  time  while  the  rapid 

1  MacWillliam,  J.  A.,  "On  the  Phenomena  of  Inhibition  in  the  Mammalian 
Heart,"  Journ.  of  Physiol,  Camb.,  1888,  ix.,  345. 


26  ETIOLOGY 

fluttering  auricular  action  continues — stimulation  of  the  inhibitory 
area  being  kept  up.  Then  after  a  time  the  ventricles  give  a  beat,  and 
after  a  long  diastolic  interval  another  beat,  and  so  on  in  slow  rhythmic 
succession,  the  inhibitory  area  being  still  under  stimulation,  .  .  .  Stimu- 
lation of  the  inhibitory  area  being  now  discontinued,  the  auricles  as  a 
rule  soon  come  to  a  state  of  rest ;  then  after  a  pause  they  beat  in  the 
ordinary  fashion  and  lead  off  the  ventricular  action  at  pretty  nearly 
the  normal  rhythm."  According  to  MacWilliam  the  inhibitory  area 
contains  many  nerve  cells  and  ganglia  and  has  numerous  nervous 
connections  establishing  a  close  relation  with  both  auricles  and 
ventricles.  The  ventricular  inhibition  resulting  from  stimulation  of 
the  inhibitory  area  was  considered  to  be  a  consequence  of  the  excita- 
tion of  certain  inhibitory  structures  within  it.  A  condition  somewhat 
similar  to  that  induced  by  experimental  stimulation  of  the  inhibitory 
area  is  observed  in  the  human  heart  when  the  auricles  are  fluttering 
and  the  vagus  is  stimulated. 

More  than  twenty  years  after  MacWilliam  first  described  auricular 
flutter,  Hirschfelder  ^  recorded  a  rapid  rhythmic  auricular  action  when 
faradic  stimulation  of  moderate  intensity  was  applied  to  the  auricular 
appendix.  Upon  stronger  stimulation  there  was  no  longer  a  co-ordinate 
contraction  of  the  whole  auricular  musculature,  but  inco-ordinate 
fibrillar  contraction. 

The  auricular  contractions  in  flutter  difler  from  those  in  fibrillation 
in  being  co-ordinate.  There  is,  however,  a  form  of  auricular  activity 
in  which  flutter  and  fibrillation  are  combined.  This  complex  form 
of  auricular  activity  was  described  by  liothberger  and  Winterberg- 
as  "  unreines  Schlagen  " — visible  auricular  contractions  involving  at 
least  the  main  mass  of  the  musculature  together  with  either  distinct 
fibrillary  movements,  especially  at  the  margins  of  the  auricles,  or  weak 
peristaltic  waves.  A  similar  condition  in  the  dog's  auricles  was  subse- 
quently described  by  Canby  Eobinson  ^  as  resulting  from  stimulation  of 
the  right  vagus  after  an  auricular  tachycardia  had  been  induced  by 
faradisation.     Korteweg  ^  has  also  described  a  form  of  auxicular  action 

1  Hirschfelder,  A.  D.,  "  Contributions  to  the  Sti^dj^  of  Auricular  Fibrillation, 
Paroxysmal  Tachycardia,  and  the  so-called  Auriculo-  (Atrio-)  ventricular  Extra- 
systoles,"  B-ull.  Johns  Hopkins  Hosp.,  Baltimore,  1908,  xix.,  322. 

2  Rothberger,  J.,  and  Winterberg,  H.,  "  Ueber  das  Elektrokardiograram  bei  Flini- 
mern  der  Vorhot'e,"  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1910,  cxxxi.,  387. 

3  Robinson,  G.  Canby,  "The  Influence  of  the  Vagus  Nerves  on  the  Faradized 
■  Auricles  in  the  Dog's  Heart,"  Journ.  of  Exp.  Med.,  New  York,  1913,  xvii.,  429. 

*  Korteweg,  A.  J.,  Arhythmie  door  Atrium-fibrillatie,  Proefschrift,  Leiden,  1913. 


EXPERIMENTAL   FLUTTER  27 

intermediate  between  fibrillation  and  flutter  as  a  result  of  vagus 
stimulation  while  the  auricles  were  being  faradised. 

In  a  later  paper  by  Canby  Robinson  ^  the  tumultuous  activity  of 
the  dog's  auricles  under  faradisation  is  described  as  consisting  of  very 
rapid  contractions  of  the  whole  auricles  (flutter)  and  simultaneous  fine 
fibrillatory  movements.  When  the  peripheral  end  of  the  right  vagus 
was  stimulated  the  general  contractions  ceased,  while  the  fibrillation 
persisted.  Moreover  the  activity  of  the  faradised  auricles  of  the  dog 
might  pass  spontaneously  into  one  closely  resembling  auricular  fiutter 
in  man,  and  this  change  might  also  occur  during  stimulation  of  the 
left  vasjus. 

The  conclusions  to  which  all  these  observations  lead  are — (1)  the 
auricular  activity  which  is  induced  by  faradisation  of  the  mammalian 
auricles  is  often  a  combination  of  flutter  and  fibrillation,  but  under 
certain  conditions  may  be  either  flutter  alone,  similar  to  that  in  man, 
or  fibrillation  alone,  as  observed  in  the  human  auricles ;  (2)  experi- 
mental flutter  may  be  changed  into  fibrillation,  or  fibrillation  into 
flutter ;  and  (3)  these  two  abnormal  forms  of  auricular  activity  in  the 
heart  of  man  or  of  other  mammals  are  closely  allied  disorders. 

We  know  that  auricular  flutter  in  the  human  heart  may  persist,  not 
merely  for  minutes  or  hours,  but  for  months  or  even  for  years.  The 
persistence  of  flutter,  however,  does  not  necessarily  imply  persistence 
of  the  exciting  cause.  In  his  original  papers  MacWilliam  stated  that 
flutter  might  continue  for  a  "  considerable  time  "  after  the  stimulation 
had  ceased.  Moreover,  according  to  Lov^n,-  Stromberg  and  Tigerstedt,^ 
and  Engelmann,'^  the  application  of  a  single  induction  shock  to  the 
great  veins,  the  sinus,  or  the  auricle  of  the  frog's  heart,  sometimes 
evokes  a  series  of  accelerated  rhythmic  beats.  The  series  starts 
abruptly,  may  last  for  two  minutes,  and  terminates  abruptly.  The 
phenomenon  is  analogous  to  the  series  of  rapid  rhythmic  ventricular 
contractions  described  by  GaskelP  as  following  the  application  of  a 
single  stimulus  to  the  auriculo-ventricular  ring  of  muscle. 

1  Robinson,  G.  Canby,  "The  Relation  of  the  Auricular  Activity  following 
Faradization  of  the  Dog's  Auricle  to  Abnormal  Auricular  Activity  in  Man," 
Journ.  of  Exp.  Med.,  New  York,  191.3,  xviii.,  704. 

-  Loven,  Mitteilungen  vom,  jjhysiol.  Lahoratorium  in  StockJiobii,  1886,  iv.,  IG. 

3  Stromberg  and  Tigerstedt,  ibid,  1888,  v.,  43. 

^  Engelmann,  Th.  W.,  "  Ueber  den  Ursprung  der  Herzbewegungen  und  die 
physiologischen  Eigenschaften  der  grossen  Herznerven  des  Frosches,"  Ardi.  f.  d.  ges. 
Phijsiol.,  Bonn,  1897,  Ixv.,  109. 

5  Gaskell,  W.  H.,  "The  Contraction  of  Cardiac  Muscle,"  Schcifers  Text-book  of 
Physiology,  Edin.  and  Loud.,  1900,  ii.,  179. 


28  ETIOLOGY 

The  close  analogy  between  auricular  flutter  induced  by  faradic 
stimulation  of  the  auricular  appendix  and  auricular  flutter  in  the 
human  heart  renders  it  probable  that  the  latter  likewise  results  from 
stimulation,  excessive  in  frequency  and  intensity,  of  a  localised  area 
in  some  part  of  the  auricular  wall.  We  do  not  yet  know  how  this 
effect  is  induced.  A  localised  inflammatory  area — an  irritative  lesion — 
in  the  sinus  node,  in  the  atrio-ventricular  node,  in  either  auricular 
appendix  or  in  the  general  auricular  musculature,  might  conceivably 
induce  auricular  flutter,  but  no  well-defined  case  with  a  single  focal 
lesion  has  yet  been  recorded.  As  tachycardia  may  be  induced  by  the 
application  of  heat  to  the  coronary  sinus,  after  destruction  of  the  sinus 
node,  Zahn  ^  has  suggested  that  the  primitive  tissue  in  the  vicinity  of 
the  coronary  sinus  may  be  the  site  of  stimulus  production  in  auricular 
flutter. 

As  the  abolition  of  vagus  control,  by  means  of  either  atropin  or 
bilateral  section  of  the  vagi,  is  accompanied  by  marked  acceleration 
of  the  auricles,  is  it  not  possible  that  auricular  flutter  may  be  due  solely 
to  loss  of  vagus  control  ?  This  hypothesis  is  improbable,  because  vagus 
stimulation,  although  retarding  the  ventricles  when  the  auricles  are  in 
flutter,  either  converts  the  flutter  into  fibrillation  or  induces  a  com- 
bination of  flutter  and  fibrillation,  but  does  not  retard  the  auricular 
beats.  Again,  as  excessive  stimulation  of  the  accelerator  nerves  can 
excite  auricular  extrasystoles,  may  it  not  be  an  important  factor  in  the 
production  of  auricular  flutter  also  ?  Possibly  this  may  be  true  in  some 
instances  when  paroxysmal  attacks  of  auricular  flutter  occur  in  a  heart 
that  is  otherwise  healthy  ;  but  when  auricular  flutter  persists  for  months 
it  is  more  likely  to  be  due  to  other  causes. 

In  the  vast  majority  of  cases  of  flutter  there  is  almost  certainly 
an  irritative  lesion  in  the  auricular  wall.  But  in  some  instances,  and 
especially  those  in  which  emotion  or  other  nervous  influences  induce 
attacks  of  auricular  flutter,  loss  of  vagus  control  and  excessive 
accelerator  stimulation  may  be  concomitant  factors. 

Age. — Auricular  flutter  has  been  recognised  in  patients  whose  ages 
have  ranged  from  5  to  74  years.  Analysing  49  cases  in  which  the  ages 
were  stated,  we  find  that  two  were  under  10  years  of  age,  four  were 
between  10  and  19,  three  between  20  and  29,  six  between  30  and  39, 
eight  between  40  and  49,  eleven  between  50  and  59,  thirteen  between 
60  and  69,  while  two  were  over  70  years  of  age. 

1  Zalin,  A.,  "  Experimentelle  Untersucliungen  iiber  ReizLildung  und  Reizleitung 
im  Atrioventrikularknoten,"  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1913,  cli.,  247. 


ETIOLOGY  29 

Sex. — About  85  per  cent,  of  the  recorded  cases  have  been  in  males. 

Arterial  Disease. — The  age  incidence,  as  recorded  above,  indicates  the 
probable  relation  between  arterial  degeneration  and  auricular  flutter. 
In  a  number  of  cases  the  radial  and  brachial  arteries  are  palpably 
thickened,  and  systolic  pressures  as  high  as  260  and  275  mm.  Hg. 
have  been  recorded. 

Other  Evidence  of  Heart  Disease. — In  nearly  all  the  cases  there  has 
been  some  evidence  of  cardiac  enfeeblement.  In  some  instances  this 
has  preceded,  but  in  others  it  has  followed,  the  attack  of  flutter.  A 
definite  history  of  antecedent  acute  rheumatism  was  elicited  in  only 
about  12  per  cent,  of  cases;  but  about  30  per  cent,  have  presented 
signs  of  mitral  disease.  In  many  of  these  cases  an  inflammatory 
process,  starting  in  the  mitral  valve,  had  probably  spread  into  the 
walls  of  the  auricles.  In  other  cases  there  was  probably  a  more  diffuse, 
sub-acute  or  chronic,  myocarditis  of  unascertained  origin. 

Auricular  flutter  has  been  known  to  arise  during  the  course  of 
diphtheria  (Cases  XLIII.  and  XLIV.),  influenza  (Cases  XXY.  and 
XXXIV.),  follicular  tonsillitis,  gastro-intestinal  catarrh,  and  other  acute 
infecti^'e  diseases.  It  is  not  improbable  that  under  such  circumstances 
there  were  inflammatory  foci  in  the  auricular  musculature.  Flutter 
may  arise  in  the  late  stages  of  exophthalmic  goitre  (Case  VII.),  and 
during  chloroform  antesthesia  (Case  IX.).  In  the  latter  connection 
it  is  of  interest  to  remember  that  this  drug  may  provoke  extra- 
systoles,  either  single  or  multiple,  and  also  fibrillation  of  the  auricles 
and  ventricles  (Levy,^  Hecht  and  Xobel-).  Of  49  cases,  there  was 
evidence  of  syphilis  in  five  (Cases  I.,  II.,  XXXVI.,  XXXVII.,  and  XLIX.), 
and  in  two  of  these  there  was  aortic  incompetence. 

1  Levy,  A.  G.,  "  The  Exciting  Causes  of  Ventricular  Fibrillation  in  Animals 
under  Chlorofoi'ni  Antesthesia,"  Heart,  Lend.,  1912-13,  iv.,  319. 

~  Hecht,  A.  F.,  and  Xobel,  E.,  "  Elektrokardiographische  Studien  iiber  Xarkose," 
Zeitschr.  f.  d.  ges.  exper.  Med.,  Berlin,  1913,  i.,  23. 


CHAPTEE  III 

MORBID  ANATOMY 

Although  the  clinical  evidence  indicates  the  existence  of  mitral  disease 
in  nearly  one-third  of  the  cases  recorded  up  to  the  present  time,  com- 
paratively little  is  known  regarding  the  morbid  anatomy  of  the  heart 
in  auricular  flutter.  It  is  evident,  however,  that  if  the  disorder  is  due 
to  a  cardiac  lesion,  this  must  be  sought  for  in  the  walls  of  the  auricles. 
Moreover,  the  experimental  and  clinical  evidence  indicates  that  the 
pathological  changes  are  probably  of  a  nature  similar  to  those  in  the 
hearts  of  individuals  who,  during  life,  had  presented  auricular  extra- 
systoles  or  auricular  fibrillation. 

In  Case  XII.,  recorded  by  George  A.  Gibson,^  the  post-mortem 
examination  revealed  a  chronic  pericarditis  which  had  led  to  oblitera- 
tion of  the  sac.  The  heart  was  dilated  and  hypertrophied,  but  there 
was  no  valvular  lesion.  On  microscopic  examination,  the  walls  of  the 
auricles  and  ventricles  were  perfectly  healthy,  save  for  a  slight  increase 
of  fibrous  tissue  close  to  the  epieardium  and  obviously  resulting  from, 
the  pericarditis.  The  atrio-ventricular  bundle  was  unduly  fibrous ;  the 
vagus  nerves  were  healthy;  the  lungs,  liver,  and  kidneys  presented 
advanced  chronic  venous  congestion,  and  in  the  liver  there  was  one 
small  hard  nodule  resembling  a  calcified  gumma. 

In  Case  III.  recent  fibrinous  pericarditis  was  found  over  the  surface 
of  the  right  auricle.  All  the  chambers  of  the  heart  were  dilated.  The 
segments  of  the  tricuspid  valve  were  shrunken  and  thickened;  the 
pulmonary  valve  was  healthy.  The  mitral  orifice  was  constricted, 
measuring  only  3  cm.  in  circumference ;  the  mitral  cusps  were  shrunken, 
thickened,  and  partially  calcified.  The  chordte  tendinese  also  were 
thickened  and  shortened,  while  the  papillary  muscles  were  fibrous. 
To  the  naked  eye  no  abnormality  was  visible  in  the  pars  membranacea 
septi.  The  aortic  cusps  were  thick  and  shrunken,  but  not  calcareous. 
The  walls  of  the  coronary  arteries  and  their  branches  contained  athero- 
matous  patches,  some  of   which  were  calcareous.      The  walls  of   the 

I  Gibson,  G.  A.,  "  A  Discussion  on  some  Aspects  of  Heart-Block,"  Brit.  Med.  Journ. 
Lond.,  1906,  ii.,  1113. 


MORBID   ANATOMY  31 

auricles  and  ventricles  presented  a  slight  degree  of  fibrosis  tiwoughout, 
while  the  lower  i)art  of  the  auricular  septum  was  involved  in  a  recent 
intlannnatory  process  spreading  into  it  from  the  anterior  cusp  of  the 
mitral  valve  (Fig.  28). 

The  sinus  node  and  the  atrio-ventricular  node  and  bundle  were  cut 
in  serial  section.  Tlie  epicardium  on  the  proximal  and  distal  sides  of 
the  cavo-auricular  junction  presented  a  considerable  infiltration  with 
lymphocytes,  together  with  a  few  plasma  cells  and  an  occasional 
polymorphonuclear    leucocyte.      This    infiltration    extended    inwards 


Fig.  28. — Inflammatory  intiltiation  of  the  auricular  musculature  near  the 
atrio-ventricular  node.    (xl33.) 

through  the  caval  and  auricular  walls,  and  involved  the  sinus  node 
and  the  numerous  nerves  and  ganglia  in  its  vicinity  (Plate  I.,  Fig.  2). 

The  atrio-ventricular  node  presented  no  abnormality  except  a  slight 
lymphocytic  infiltration,  which  was  of  lesser  severity  than  that  else- 
where in  the  auricular  septum.  The  greater  part  of  the  main  stem 
of  the  atrio-ventricular  bundle  was  entirely  free  of  inflammatory  or 
degenerative  changes.  A  sub-acute  inflammatory  process,  however, 
extended  inwards  from  the  septal  cusp  of  the  tricuspid  valve  so  as 
to  involve  the  terminal  portion  of  the  bundle  and,  to  a  lesser  extent, 
the  initial  portions  of  both  its  branches. 

It  was  evident,  therefore,  that  the  various  pathological  changes  in 
this  heart  were  due  to — (1)  atheroma  of  the  coronary  arteries ;  (2)  endo- 


32  MORBID   ANATOMY 

carditis  spreading  into  the  auricular  septum  from  the  mitral  valve ;  (3) 
endocarditis  extending  inwards  from  the  tricuspid  valve  so  as  to  involve 
the  atrio-ventricular  bundle  and  its  branches  ;  and  (4)  acute  pericarditis 
implicating  the  sinus  node  and  the  abundant  nerve  elements  in  its 
vicinity. 

In  Case  VII.  (exophthalmic  goitre  and  myocarditis)  the  post-mortem 
examination  was  made  by  Dr.  James  Miller.  The  form  of  the  heart 
was  found  to  be  similar  to  that  outlined  in  an  orthodiagram  seventeen 
days  before  death.  The  maximum  transverse  diameter  was  10'5  cm.  ; 
the  long  diameter  from  the  superior  cavo-auricular  junction  to  the  apex 
was  13  cm.  The  left  auricle  and  its  appendix,  which  had  not  been 
visible  on  the  screen,  were  not  exposed  until  the  heart  was  rotated 
to  the  right  on  its  long  axis. 

The  pericardium  was  healthy.  The  jugular  veins,  the  venee  cavse, 
and  the  right  auricle  were  dilated.  The  v/all  of  the  latter  chamber  was 
thin,  and  on  microscopic  examination  marked  diffuse  inter-fascicular 
fibrosis  was  seen.  In  some  of  the  pectinate  muscles  the  muscle  fibres 
had  lost  their  striation,  and  the  nuclei  failed  to  take  the  stain,  but 
there  was  very  little  infiltration  with  inflammatory  cells.  The  tricuspid 
orifice  measured  14-5  cm.  in  circumference ;  its  valve  was  healthy.  The 
cavity  of  the  right  ventricle  was  dilated,  and  its  wall  slightly  hyper- 
trophied.  Sections  taken  from  the  conus  arteriosus  presented  no 
abnormality  except  slight  increase  of  connective  tissue  between  the 
muscle  fibres.  The  pulmonary  orifice  measured  9  cm.  in  circumference, 
and  its  valve  was  healthy. 

The  cavity  of  the  left  auricle  was  dilated  and  the  endocardium 
thickened.  Its  wall  was  very  thin,  and  on  microscopic  examination 
presented  considerable  diffuse  inter-fascicular  fibrosis ;  but  no  lympho- 
cytic infiltration,  and  none  of  the  degenerative  changes  observed  in  the 
wall  of  the  right  auricle,  were  detected.  The  mitral  orifice  measured 
12  cm.  in  circumference;  the  valve  segments  were  somewhat  thick 
and  fibrous.  The  muscle  of  the  left  ventricle  was  of  dark  colour 
and  somewhat  soft.  Microscopic  examination  revealed  small  patches 
of  fibrosis  throughout  the  ventricular  wall,  but  particularly  in  the 
apices  of  the  papillary  muscles  and  in  the  sub-endocardial  layers  of 
the  columnse  earner.  The  aortic  orifice  measured  8  cm.  in  circum- 
ference; the  basal  portions  of  the  cusps  were  thickened,  but  the 
valve  was  competent  to  the  water  test. 

The  pars  membranacea  septi  was  large,  thin,  and  free  from  inflam- 
matory reaction.     The  auricular  septum  in  front  of  the  mouth  of   the 


MOKlill)   ANATOMY  33 

oorouary  sinus  was  likewise  healthy.  The  atiio-veiitiicular  node,  the 
bundle  and  the  upper  portions  of  both  branches,  were  cut  serially. 
The  only  abnormality  was  a  very  slight  lymphocytic  infiltration  in 
some  parts  of  the  bundle  and  adjacent  ventricular  muscle.  The  atrio- 
ventricular node  and  both  branches  of  the  bundle  were  healthy. 

The  lungs  and  the  abdominal  viscera  were  markedly  congested. 
The  microscopic  appearances  of  the  enlarged  thyroid  gland  w^ere 
characteristic  of  exophthalmic  goitre.  The  acini,  of  irregular  shape, 
were  lined  by  columnar  cells  and  contained  colloid  material,  while 
the  amount  of  interstitial  connective  tissue  was  scanty. 

In  Case  XI.  the  post-mortem  examination  was  made  by  iJr. 
^lurray  Drennan,  The  heart  was  greatly  enlarged,  and  all  the 
chambers  were  dilated.  The  walls  of  both  auricles  were  thin,  and 
the  right  auricular  appendix  contained  several  adherent  ante-mortem 
thrombi.  The  tricuspid  orifice  was  dilated,  measuring  15  cm.  in 
circumference ;  the  pulmonary  orifice  measured  8  cm.,  the  mitral 
12  cm.,  and  the  aortic  8  cm.  in  circumference.  The  wall  of  the  left 
ventricle  was  slightly  hypertrophied.  There  were  only  two  aortic 
cusps ;  both  were  large,  thickened,  and  had  calcareous  nodules  on  their 
aortic  surfaces,  but  the  valve  was  competent.  The  wall  of  the  aorta 
and  the  coronary  arteries  showed  nodular  atheroma.  There  was 
resolving  pneumonia  in  the  lower  and  middle  lobes  of  the  right 
lung  and  in  the  lower  lobe  of  the  left  lung;  the  liver  and  spleen 
showed  chronic  venous  congestion ;  and  the  kidneys  were  cystic. 
Xeither  the  vagi  nor  the  cervical  sympathetic  presented  any  change 
throughout  their  entire  course. 

Microscopic  examination  revealed  a  very  slight  degree  of  fatty 
degeneration  of  the  ventricular  niuscle,  and  a  slight  fibrosis  which  was 
more  marked  in  the  auricles  than  in  the  ventricles.  An  acute  cellular 
infiltration  was  seen  in  the  lowest  part  of  the  auricular  septum 
posteriorly,  but  both  nodes,  the  bundle,  its  branches,  and  the  tissues 
at  the  mouth  of  the  coronary  sinus  were  healthy. 

In  Case  XLIII.,^  one  of  diphtheria  with  terminal  auricular  fiutter, 
the  musculature  of  the  auricles  and  ventricles  had  undergone  fatty 
degeneration,  and  in  the  walls  of  the  ventricles  there  was  a  pronounced 
degree  of  interstitial  myocarditis.  The  atrio-ventricular  node  and  bundle 
were  healthy,  as  were  also  the  valves. 

In  Case  XLIV.^  auricular  fiutter  supervened  on  the  eleventh  day  of 

1  Hume,  \X.  E.,  "A  Polygiaphic  Study  of  Four  Cases  of  Diphtheria  with  a  Patho- 
Ljgical  Examination  of  Three  Cases,"  Heart,  Lond.,  191.3-14,  v.,  25. 


34  MOEBID   ANATOMY 

an  attack  of  diphtheria,  two  days  before  death  (see  p.  77).  All  the 
chambers  of  the  heart  were  found  to  be  dilated,  but  the  valves  were 
healthy;  the  myocardium  was  pale  and  friable;  the  right  auricular 
appendix  was  filled  with  an  ante-mortem  thrombus.  The  sinus  node 
was  infiltrated  with  mononuclear  cells  of  the  formative  type;  the 
capillaries  within  the  node  were  engorged,  and  haemorrhages  had  taken 
place  from  them ;  the  muscle  fibres  of  the  sinus  node  were  in  a  state 
of  granular  degeneration.  The  atrio- ventricular  node  was  normal  except 
for  slight  engorgement.  The  bundle  and  its  branches  were  perfectly 
normal ;  the  auricular  musculature  presented  slight  fatty  degeneration ; 
the  ventricular  musculature  presented  intense  fatty  degeneration  but  no 
interstitial  myocarditis. 

In  conclusion,  it  is  evident  that  the  number  of  post-mortem  examina- 
tions is  still  too  small  to  permit  of  any  final  conclusions  regarding  the 
condition  of  the  heart  in  auricular  flutter.  The  available  evidence 
nevertheless  demonstrates  that  flutter  may  be  associated  with  wide- 
spead  acute  or  sub-acute  inflammation  and  degenerative  changes  in  the 
auricular  musculature,  and  that  these  changes  may  involve  both  nodes 
and  the  bundle.  These  changes  may  arise  in  the  course  of  an  acute 
infective  disease.  More  frequently  they  are  due  to  disease  of  the 
coronary  vessels  or  to  inflammation  extending  into  the  muscle  from  the 
pericardium  or  from  the  mitral  and  tricuspid  valves. 


CHAPTER  IV 

RECORDS    OF   CASES 

Eleven  cases  that  have  come  under  my  own  observation  will  first 
be  described,  and  thereafter  other  cases  recorded  in  the  literature 
will  be  referred  to. 

Case  I. — Auricular  Flutter  with  Complete  Heart-block  ;  in  Two 
Initial  Attacks  of  Flutter  the  Maximum  Auricular  Rates 
were  275-5  AND  300  per  Minute  respectively;  a  Third 
Attack  Persisted  for  nearly  Five  Years;  between  the 
Attacks  the  Auricles  beat  Slowly  and  Irregularly.^ 

The  patient,  a  cabman,  was  aged  55  when  seen  for  the  first  time 
in  May  1904.  His  wife  had  two  children,  who  died  in  infancy  of 
diphtheria  and  pneumonia  respectively,  and  three  abortions.  He 
denied  syphilis,  but  when  his  blood  serum  was  tested  in  1909  it  gave 
a  positive  Wassermann  reaction. 

When  aged  16  he  suffered  from  inflammation  of  the  kidneys.  At 
the  age  of  50  he  became  affected  with  muscular  rheumatism,  and 
eighteen  months  later  with  bronchitis  and  dyspnoea.  In  November 
1903  he  suffered  from  acute  lobar  pneumonia,  and  subsequently  became 
more  short  of  breath  and  less  able  for  his  work.  He  then  began  to 
experience  attacks  of  faintness  and  giddiness  on  exertion  two  or  three 
times  a  week.  He  said  the  attacks  were  "  a  sort  of  sudden  blindness, 
and  he  had  to  hold  on  to  a  railing  lest  he  should  fall."     Each  attack 

1  Records  of  tliis  case  are  contained  in  the  following  papers  : — 

Cowan,  J.,  and  Ritchie,  W.  T.,  "  Coupled  Rhythms  of  the  Heart,"  Quart.  Journ. 
of  Med.,  Oxford,  1910-11,  iv.,  55  (Case  II.,  pp.  60,  61). 

Gibson,  G.  A.,  "Bradycardia,"  Edin.  Med.  Journ.,  Edin.,  1905,  (N.  S.),  xviii.,  9 
(Case  III.). 

Gibson,  G.  A.,  "  A  Discussion  on  some  Aspects  of  Heart-block,"  Brit.  Med.  Journ., 
Lond.,  1906,  ii.,  1113. 

Jolly,  W.  A.,  and  Ritchie,  W.  T.,  "Auricular  Flutter  and  Fibrillation,"  Heart, 
Lond.,  1910-11,  ii.,  177. 

Ritchie,  W.  T.,  "  Complete  Heart-block,  with  Dissociation  of  the  Action  of  the 
Auricles  and  Ventricles,"  Proc.  Roy.  Soc.  of  Edin.,  1905,  xxv.,  1085. 

Ritchie,  W.  T.,  "Further  Observations  on  Auricular  Flutter,"  Quart.  Joiirn.j)/ 
Med.,  Oxford,  1913-14,  vii.,  1. 


36 


EECOEDS   OF   CASES 


lasted  as  a  rule  for  ten  or  fifteen  minutes.     He  had  never  actually  lost 
consciousness. 

On  examination  he  was  a  well-nourished  man,  somewhat  cyanotic, 
but  not  dropsical.  The  walls  of  his  radial  and  brachial  arteries  were 
moderately  and  diffusely  thickened.  The  arterial  pulse  was  of  large 
volume  and  rhythmic  at  a  rate  of  31-36  beats  per  minute.  The  heart 
was  greatly  enlarged,  as  is  evident  from  the  orthodiagraphic  record 
obtained  on  the  16th  August  1911  (Fig.  29).  The  forcible  cardiac 
impulse,  which  had  the  same  rate  and  rhythm  as  the  arterial  pulse, 
could  be  seen  and  felt  in  the  sixth  intercostal  space  as  far  out  as  12  cm. 
from  the  mid-sternal  line.     The  position  of  the  apical  impulse  was  not 


Fig.  29.— Orthodiagram  of  Case  I.  The  heart  is  greatly 
enlarged  and  the  aorta  is  prominent.  The  position 
of  the  supra-sternal  notch,  the  nipples,  and  the  apex- 
beat  is  indicated. 


influenced  by  changes  of  posture;  the  epigastrium  was  indrawn  with 
each  ventricular  systole,  and  Broadbent's  sign  was  well  marked.  On 
auscultation  a  loud  blowing  systolic  murmur  of  mitral  origin  was 
audible,  but  no  other  murmur  could  be  heard,  and  no  sounds  were 
detected  during  the  long  diastolic  pauses.  The  second  sound,  especi- 
ally at  the  aortic  area,  was  clear  and  accentuated.  It  was  therefore 
evident  that  the  patient  was  affected  with  mitral  incompetence, 
chronic  adhesive  mediastino-pericarditis,  and  arterio-sclerosis.  The 
lungs  presented  some  vesicular  emphysema  and  bronchitis,  but 
examination  of  the  abdomen,  blood,  urine,  and  nervous  system 
revealed  no   abnormality. 

The    rate   of    the    jugular    pulsations   was    observed   to   be  more 


CASE   I. 


37 


rapid  than  that  of  the  arterial  pulse.  Complete  dissociation  of  the 
ventricular  rhythm  from  that  of  the  auricles  was  first  demonstrated  in 
polygraph  tracings  taken  by  Dr.  Oliphant  Xicliolson  in  1904.  Some  of 
these  tracings  were  reproduced  in  Dr.  G.  A.  Gibson's  paper  in  1905.  In 
other  tracings  that  I  obtained  by  means  of  the  Knoll-Hering  polygraph 
daring  the  period  from  26th  March  until  16th  June  1905,  complete 
heart-block  w^as  always  demonstrated,  the  rates  of  the  auricles  and 
ventricles    being    50-7-70-5    and    31-1-35-7    per    minute    respectively 


Fig.  30.— Complete  heart-block.    Jugulo-carotid,  brachial,  and  apical  tracings.    The  time  record  is 
0-2  second.    (Case  I.  before  the  onset  of  auricular  flutter.) 


(Fig.  30).  The  patient's  history  was  uneventful  until,  on  the  2nd  June 
1905,  while  cleaning  a  window^  he  had  a  "giddy  attack"  and  fell  from 
a  ladder.  He  did  not  hurt  himself.  This  was  the  last  manifestation  of 
the  Adams-Stokes  syndrome.  On  the  following  day  his  ventricular  rate 
was  40  per  minute  after  he  had  walked  a  distance  of  one  mile,  and 
34-75  per  minute  after  resting  for  two  hours.  On  the  16th  June  the 
auricles  were  beating  somewhat  irregularly  at  a  rate  of  60'71  per 
minute,  while  the  ventricular  beats  were  rhythmic  at  a  rate  of  32  per 
minute.  On  the  19th  June  1905,  when  the  patient's  heart  was 
examined  by  radioscopy,  his  right  auricle  was  observed  to  be  beating 
rhythmically  about  60  times  per  minute,  and  to  have  a  rhythm 
independent  of  the  slower  ventricular  beats. 


38 


EECOEDS   OF   CASES 


TABLE  I. 


Rate  per 

Minute. 

Auricles. 

Ventricles. 

1905.  March 

26 

64-78 

33-80 

Both  auricles  and  ventricles  are  beat- 
ing rhythmically. 

April 

16 

70-5 

32-9 

39 

30 

66-8 

35-7 

May 

19 

50.76 

32-30 

Auricles  slightly  arrhythmic. 

June 

2 

t  .  • 

Syncopal  attack.     Fell  from  ladder. 

)j 

9 

65-'8 

31-14 

Auricles  somewhat  arrhythmic. 

16 

60-71 

32 

J5 

19 

... 

Examined  by  Rontgen  rays.  Auricles 
beating  60  times  per  minute. 

)5 

20 

Patient  began  to  take  jJq  grain  of 
atropin  sulphate  thrice  daily. 

23 

273-03 

34-88 

274-73 

36-58 

Ten  minutes  after  Jg  grain  of  atropin 
sulphate. 

99 

27 

Atropin  stopped. 

J9 

30 

275-5 

so-b 

Both  auricles  and  ventricles  are  beat- 
ing rhythmically. 

July 

8 

270-77 

30-77 

October 

14 

43-70 

31-57 

1906.  June 

3 

290-90 
300-0 

32-96 
33-80 

1908.  May 

28 

57-39 

31-30 

Ventricles  are  arrhythmic. 

August 

25 

53-33 

33-60 

Both  auricles  and  ventricles  are  some- 
what arrhythmic. 

November  19 

291-89 

33-61 

Both     auricles     and     ventricles     are 

rhythmic. 

1? 

19 

272-72 

33-33 

J) 

19 

267-85 

34-09 

21 

272-72 

33-33 

1909.  February 

22 

268-75 

35-29 

A  few  ventricular  extrasystoles. 

Marcb 

8 

255-55 

42-85 

Both  auricles  and  ventricles  are 
rhythmic. 

July 

28 

260-86 

31-91 

August 

19 

262-5 

33-3 

After  bilateral  pressure  on  the  vagi. 

19 

257-0 

34-2 

After  exercise. 

5> 

20 

234-63 

31-91 

Both  auricles  and  ventricles  are 
rhythmic. 

91 

25 

56 

Group-beating  of  ventricles. 

59 

26 

252-63 

34-42 

A  few  ventricular  extrasystoles. 

September  20 

276-9 

32-4 

Both  auricles  and  ventricles  are  beat- 

ing rhythmically. 

15 

30 

261-11 

56-7 

Group-beating  of  ventricles. 

October 

4 

260-86 

58-9 

55 

9 

268-1 

41-02 

10.30  A.M.     Ventricular  arrhythmia. 

55 

9 

41-74 

10.40  A.M. 

J? 

9 

10.51  A.M.  Jg-  grain  of  atropin  sul- 
phate subcutaneously. 

55 

9 

263-8 

10.56  A.M. 

5) 

9 

44-21 

10.57  A.M. 

5} 

9 

44-6 

11.3  A.M. 

55 

9 

268-6 

44-44    . 

11.11  A.M. 

5) 

9 

48-2 

11.12  A.M. 

CASE   I. 


39 


Ratk  per 

MiNOTE. 

Auricles. 

Ventricles. 

1909.  October        9 

45-2 

11.19  a.m. 

9 

26'6'8 

44-0 

11.27  A.M. 

14 

272-7 

51-5 

Group-beating  of  ventricle.?.  Has 
been  taking  digitalis  for  five  days. 

November  13 

Ventricles  beating  rliythmically. 

90 

251-18 

6315 

(iroup-beating  of  ventricles. 

29 

Digitalis  stopped. 

December     2 

250-0 

34-6 

Ventricular  extrasystoles. 

1910.  January      13 

265-55 

37-50 

Ventricular  arrhythmia. 

February      3 

280-03 

35-55 

Ventricles  more  rhythmic. 

10 

252-99 

31-92 

Ventricles  rhythmic. 

March         24 

258-46 

32-43 

Occasional  ventricular  extrasystoles. 

24 

246-77 

32-70 

April          28 

254-23 

36-20 

Ventricles  rhythmic. 

May            16 

264-5 

35-5 

August         8 

251-35 

34-61 

Ventricles  rhythmic. 

Se])tember  16 

250-0 

55-3 

Group-beating  of  the  ventricles. 

October      10 

253-8 

60-5 

j>                   1)               ?) 

November  16 

250-0 

55-3 

55                                      55                              55 

December  27 

250-0 

50-5 

Neither  right  nor  left  vagus  compres- 
sion retards  auricles  or  ventricles. 

1911.  February      8 

250-0 

62-5 

Group-beating  of  the  ventricles. 

April          24 

36-5 

Ventricles  rhythmic. 

27 

252-6 

41-5 

Ventricles  rhythmic.  Before  inhala- 
tion of  amyl  nitrite. 

27 

256-4 

41-4 

After  inhaling  amyl  nitrite  for  four 
minutes. 

May            11 

45 

Maximum  systolic  pressure,  165  ;  dias- 
tolic pressure,  125  mm.  Hg. 

July            10 

277-7 

32-4 

Respiratory  rate  the  same  as  the 
ventricular. 

July            17 

267-0 

33-5 

Ventricles  rhythmic. 

August        18 

242-8 

37-9 

55                               55 

October      26 

232-7 

33-9 

55                                 55 

November    1 

232-4 

33-6 

55                                 55 

15 

229-5 

32-0 

Ventricles  rhythmic.  Has  been  taking 
30  minims  of  tincture  of  squill  daily 
since  19th  October. 

December     8 

244-9 

37-4 

Ventricles  rhythmic. 

1912.  January        4 

244-9 

52-4 

Ventricles  arrhythmic. 

8 

244-9 

39-3 

Ventricular  beats  often  coupled. 

August       22 

244-8 

55-7 

Plate  IX.,  Fig.  36. 

September  25 

244-4 

38-2 

Plate  IX.,  Fig.  38. 

October      22 

242-5 

38  0 

A'entricles  arrhythmic. 

December  16 

235-7 

32-7 

Ventricles  rhythmic  except  for  an 
occasional  premature  beat. 

1913.  March         10 

190-5 

44-8 

Group-beating  of  the  ventricles. 

April           11 

194-8 

1 

47          j 

1 

Numerous  premature  ventricular 
beats. 

24 

194-8 

35-7       ! 

Ventricles  rhythmic. 

May               2 

201-0 

34-9 

55                                    55 

9 

192-6 

42-4 

Group-beating  of  the  ventricles. 

13 

187-3 

31-7 

Ventricles  rhythmic. 

19  1 

192-8 

33-3       1 

2.32  P.M. 

19  i 

189-0 

40-3       ! 

2.35  P.M. 

19  i 

189-4 

42-4 

2.40  P.M. 

40 


EECOEDS   OF   CASES 


Raie  pkr 

MlXUTE. 

Auricles. 

Ventricles. 

1913.  May            19 

2.42  P.M.    0-03  grain  atiopin  sulphate 
subcutaneously. 

19 

192-8 

37-9 

2.52  P.M. 

19 

193-5 

40-6 

3.2  P.M. 

19 

195-9 

41-4 

3.8  P.M. 

19 

197-8 

42-0 

3.14  P.M. 

21 

190-5 

31-3 

11.0   A.M. 

11.5  A.M.  0*001  gramme  stroplianthin 
(Boehringer)  intravenously. 

21 

92-1 

29-0 

1.35  P.M. 

21 

119-6 

41-0 

1.40  P.M. 

July            15 

201-6 

40-6 

An  occasional  ventricular  extrasystole. 

22 

247-8 

51-4 

Ventricles     arrhythmic    and    extra-  ; 

systoles. 

29 

235-7 

39-8 

Ventricles  rhythmic. 

August       15 

237-9 

38-1 

An  occasional  ventricular  extrasystole. 

29 

240-0 

38 

Admitted  to  hospital  with  congestion 
at  base  of  left  lung. 

30 

236-8 

41 

31 

233-1 

43 

Began    to     take     digitalis     tincture. 
Ventricles  irregular. 

September    1 

232-2 

38-3 

2 

230.7 

34 

Ventricles  almost  wholly  rhythmic. 

3 

233-7 

34-6 

Ventricles  rhythmic. 

4 

240-0 

34-2 

5 

230-7 

31-9 

Digitalis    stop^^ed.     Has    taken    180 
minims. 

11 

57-1 

32-9 

19 

Left  hospital,  much  improved. 

22 

63-6 

33  3 

October        2 

244-9 

36-8 

14 

69-5 

38-0 

Both  auricles  and  ventricles  irregular. 

15 

45-6 

41-4 

?'                  '»                    )) 

17 

52-2 

42-3 

■>■>                                   It                                        )5 

21 

71-4 

38-4 

fi                                  J?                                        ?) 

„            31 

58-7 

36-3 

1"                                       51                                             1? 

November  21 

236-0 

38 

Auricular  deflexions  are  rhythmic  and 
diphasic. 

28 

225-5 

37-2 

Auricular  deflexions  are  rhythmic  and 
diphasic. 

December     4 

227-5 

32-6 

8 

237 

35-3 

Ventricles  rhythmic. 

10 

223-2 

38 

Ventricles  somewhat  arrhythmic. 

1914.  January      14 

232-9 

48-7 

5)                             )»          _                         5) 

23 

232-4 

39-8 

Ventricles  rhythmic. 

Four  days  later  (23rd  June  1905)  the  auricles  were  fluttering. 
The  patient  had  been  taking  yJo  grain  of  atropin  sulphate  thrice  daily 
for  three  days.  He.  felt  better,  and  was  less  breathless  than  formerly, 
but  for  the  first  time  the  rate  of  his  auricles  was  observed  to  be 
greatly  accelerated,  the  beats  being  rhythmic  at  a  rate  of  273'03  per 
minute,   while   the   ventricular   rate   was    34"88.     Ten    minutes   after 


CASE   I.  41 

'^jy  grain  of  atropin  sulpliate  had  been  given  subeutaneously  the 
aunciilar  and  ventricular  rates  were  274*73  and  36"58  per  minute 
respectively.  He  continued  to  take  yjiy  grain  of  atropin  sulpliate 
tlu'ice  daily  until  the  27tli  June,  when  he  began  to  take  15  minims 
of  strophanthus  tincture  daily.  On  the  30th  June,  after  55  minims  of 
this  tincture  had  been  taken,  he  said  he  felt  "  all  right " ;  the  auricular 
and  ventricular  rates  were  275'5  and  30-0  per  minute  respectively. 
On  the  8th  July  1905,  a  week  after  he  had  ceased  taking  strophanthus, 
he  felt  well.  The  cyanosis  had  disappeared.  The  auricular  and  ven- 
tricular rates  were  270*77  and  3077  per  minute  respectively. 

He  felt  so  well  that  he  was  able  to  follow  his  occupation  as  a  coach- 
man in  a  country  hotel,  driving  carriages,  grooming  horses,  and  cleaning 
the  stalls  and  harness.  Whether  his  auricles  were  still  fluttering,  I 
cannot  say.  But  after  being  thus  engaged  for  a  month,  he  began  to 
be  troubled  with  vomiting,  which  was  probably  induced  by  alcoholic 
excess.  When  he  returned  to  town,  feeling  weak  and  troubled  with 
cough,  but  neither  cyanotic  nor  dropsical,  his  ventricles  were  beating 
rhythmically  at  a  rate  of  34'75  per  minute.  On  the  next  occasion 
when  records  of  his  auricular  action  were  obtained,  namely,  on  the 
14th  October  1905,  the  auricular  flutter  had  disappeared  and  had 
been  replaced  by  an  infrequent  auricular  rate  of  43'70,  while  the 
ventricular  rate  was  31'57  per  minute.  During  the  following  winter 
the  patient  felt  well  and  able  for  any  work  he  could  have  obtained. 
His  ventricular  rate  was  not  observed  to  rise  above  37  nor  to  fall 
below  32*5  per  minute. 

On  the  3rd  June  1906,  without  the  patient  having  experienced 
any  particular  subjective  phenomena,  the  auricular  flutter  was  found 
to  have  recurred.  The  auricular  rate  was  then  290'9-300  per  minute. 
In  May  and  August  1908  the  auricular  rate  had  again  fallen  to 
53-57  per  minute.  On  the  19th  November  1908,  however,  the 
auricles  were  again  fluttering  at  a  rate  of  267*8-291'8  per  minute. 
In  all  the  records  taken  from  that  day  until  July  1911,  the  auricular 
rate  was  usually  between  250  and  275  per  minute,  and  only  once  fell 
as  low  as  234'6.  During  the  succeeding  period  of  sixteen  months 
(August  1911  until  December  1912)  the  recorded  auricular  rates 
never  rose  above  244*9  nor  fell  below  229  per  minute.  Thus  on 
every  occasion  during  a  period  of  four  years,  the  flutter  was  recorded 
(Table  I.).  Subsequently  the  auricular  rate  was  usually  about  189-195 
per  minute.  Still  later,  short  periods  of  flutter  at  a  rate  of  230-244 
alternated  with  others  during  which  the  auricular  rate  was  infrequent 
(45-71  per  minute). 


42 


EECOEDS   OF   CASES 


During  the  prolonged  attack  of  flutter,  the  patient  was  somewhat 
breathless  and  cyanotic  from  time  to  time,  and  the  lower  lobe  of  the  left 
lung  shewed  transient  congestion  and  oedema.  The  urine  eventually 
contained  a  constant  trace  of  albumin  with  hyaline  and  granular 
tube-casts.  There  has  never  been  any  oedema  of  the  limbs,  and  the 
patient  is  still  able  to  walk  to  hospital,  a  distance  of  about  two  miles 
from  his  home,  without  becoming  unduly  fatigued  or  breathless. 

Polygraph  Tracings. — When  the  auricles  were  fluttering,  faint  yet 
distinct  rapid  pulsatile  movements  could  usually  be  seen  in  the 
jugular  veins  if  the  patient  were  in  the   recumbent   posture.      These 


Fig.  31. — Auricular  flutter  and  complete  heart-block.  The  jugulo-carotid  and  apical  traeing.s  present  a  series  of 
rhythmic,  positive  waves,  the  rate  of  which  is  about  255  per  minute.  The  ventricles  contract  rhythmically 
32 '2  times  per  minute.     Heart,  vol.  ii.) 

movements  were  recorded  graphically  on  many  occasions.  Fig.  31 
shows  the  jugulo-carotid,  apical  and  brachial  tracings  recorded  simul- 
taneously from  this  case  in  1905.  The  rhythmic  beats  of  the  auricles 
at  a  rate  of  255  per  minute  are  represented  by  rhythmic  waves,  a, 
in  the  venous  and  apical  tracings.  The  ventricles  were  contracting 
rhythmically  at  a  rate  of  3 2 "2  per  minute. 

Electrocardiogravis. — The  first  electrocardiograms  from  this  patient 
were  recorded  by  Jolly  in  1909.  He  demonstrated  that  the  rhythmic 
auricular  deflexions  (Fig.  32)  were  brought  to  light  more  clearly  when 
the  tension  of  the  fibre  was  reduced  until  its  deflexion  time  was  0'031 
second  than  when  its  tension  was  greater  and  its  deflexion  time  was 
0*022  second.     He  also  proved  that  these  rhythmic  auricular  deflexions 


I'LATK  Vil. 


n 


/  ssc. 


Fio.  32.— Auricular  flutter,  at  a  rate  of  270  per  minute,  and  complete  heart-block.    Ca.se  I.     Derivation  HI. 

(From  Hc.i.rt,  vol.  ii.) 


Fig.  33. — Auricular  flutter,  at  a  rate  of  24-5  per  minute,  and  complete 
heart-block.  The  .second  ventricular  beat  is  an  extra.systole. 
Case  I.  (21st  Julv  1913).     Derivation  I.     l-o  cm.  =1  millivolt. 


Fig.  34.— Case  I.  Tlie  flutter  has  ceased  and  the  auricles  are  beating  at  a  rate  of  t;5-5  per  minute.  ITie 
auricular  deflexions  are  diphasic.  Tlie  block  is  .still  complete.  Derivation  II.,  14th  October  1913. 
1'5  cm.  =1  millivolt. 


p-E 


PLATK    IX. 


^^  Sf"""'^'^,  V*^.  V^ 


Fio.  30. 


Fin.  37. 


^       A  A 


1 1 1 1 1 1 1 1 11 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 : 1  'I  '^ 

iiitJIiiiiiiiiiiiiiiii iMiiiiiiiiiiiiinii! uuiiuiuiiiiiiuiiiitmiiuuiuiuiuaaiuiuiuuuiiuui 


Fic.  38. 


Fig.  39. 


'WV^  ^^V^^J'^^sJ^.^J^ 


'^w 


( 

llllllllllllllllllllllllllllllllllllliiliiuiiMMiinninii.i. 

IlllMiiiliMiMiiiiiiiiiiniiiMiiiMMiitiiiiniiiiiiiiiiiiMiniliii 


Fics.  3.J,  3S,  4ri.— Auricular  flutter  and  complete  heart-block.  Case  I.  Derivations  I.  (il-2nd  August  1012),  II.  (I'oth  September 
1012),  and  III.  (2oth  September  1012)  respectively.  The  auricular  rate  is  244-S,  244-4,  and  244-4  per  minute,  and  the  total 
value  of  the  auricular  deflexions  about  70,  200,  and  200  microvolts  respectively.  In  Figs.  3S  and  40  the  auricular  deflexions 
aie  diphasic.     1-5  em.  =  1  millivolt. 

Figs.  37,  30.41.— Case  I.  Derivations  I.,  II.,  and  III.  respectively.  In  Fig.  37  the  auricular  deflexions  are  inconspicuous.  In 
Figs.  30  and  41  the  auricular  rates  are  104  S  and  107-7  per  minute  respectively,  and  the  value  of  the  auricular  deflexions  is 
about  100  microvolts  (11th  April  1013).    1-5  cm.  =1  millivolt.    {Quart.  Join  n.  yM.,  vol.  vii.) 


CASE   I.  43 

did  not  represent  tremor  of  skeletal  muscles,  ventricular  beats,  contrac- 
tions of  caval  musculature  at  a  greater  rate  than  that  of  the  auricles, 
or  fibrillar  contraction  of  the  auricular  musculature.  The  deflexions 
were  recognised,  therefore,  to  be  rhytlimic  co-ordinate  contractions  of 
the  auricular  musculature.  By  derivation  I.  each  auricular  contraction 
was  represented  by  a  simple  upward  deflexion.  By  derivations  II.  and 
III.  each  auricular  deflexion  was  diphasic,  being  composed  of  an  initial 
deflexion  upwards  succeeded  after  an  interval,  during  which  the  shadow 
of  the  fibre  traced  a  horizontal  line,  by  a  downward  deflexion.  The 
upward  deflexion  was  less  acute  than  the  downward.  The  duration 
of  the  former  was  about  0*1  second,  that  of  the  latter  0"059  second. 
As  recorded  by  derivation  I.,  the  auricular  deflexions  were  shown  to 
have  a  value  of  about  60  microvolts,  as  compared  with  100-200  micro- 
volts in  the  case  of  the  auricular  deflexions  of  a  healthy  human  heart. 

In  all  the  subsequent  electrocardiograms  until  December  1912,  the 
form  of  the  auricular  deflexions  as  recorded  by  each  derivation  was 
constant.  Derivation  I,  gave  a  simple  rise  and  fall,  with  a  value  of 
60-70  microvolts.  Derivations  II.,  III.,  and  lY.  yielded  diphasic  curves 
with  an  initial  upward  deflexion  and  a  total  value  of  about  200  micro- 
volts (Figs.  36,  38,  -40).  Atropin  did  not  accelerate  the  auricular  rate, 
and  compression  of  the  right  or  left  vagus  in  the  neck  did  not  arrest,  or 
even  retard,  the  auricles  (Plate  VIII.,  Fig.  35). 

During  a  period  of  about  three  months  in  the  spring  of  1913  the 
auricular  rate  was  as  a  rule  only  about  190-194  per  minute,  with  a 
maximum  of  201  per  minute.  Subsequently  a  more  frequent  rate 
(223-247)  was  again  maintained.  In  contrast  with  the  antecedent  and 
subsequent  auricular  flutter,  the  less  frequent  auricular  action  was 
represented  by  deflexions  of  lesser  amplitude,  and  by  derivations  II. 
and  III.  they  were  no  longer  uniformly  diphasic  (Figs.  37,  39,  41). 
Further,  the  auricular  action  could  then  be  accelerated  by  means  of 
atropin  and  retarded  by  means  of  strophanthiu  administered  intra- 
venously. It  is  probable  that  the  true  auricular  flutter,  which  was 
not  under  vagus  control,  and  the  less  frequent  auricular  tachysystole, 
were  not  initiated  at  the  same  site  in  the  auricular  wall.  The  evidence 
at  present  available  suggests  that  the  chronotropic  influence  of  the  vagus 
upon  the  auricles  is  exerted  mainly  through  the  sinus  node,  and  conse- 
quently the  site  at  which  the  slower  auricular  rhythm  was  initiated  was 
probably  nearer  the  sinus  node  than  that  of  the  true  flutter. 

"When  the  auricles,  in  October  1913,  again  beat  slowly  and  irregu- 
larly their  electrocardiographic  deflexions  were  of  more  normal  form 
than  when  the  auricles  were  in  flutter  (Plate  YIL,  Fig.  34). 


44 


EECOEDS   OF   CASES 


The  Ventricles. — For  five  years  after  the  heart-block  was  recognised 
the  ventricular  rate  was  constantly  about  32-36  per  minute,  and  the 
rhythm  was  absolutely  regular.  In  March  1909  a  few  ventricular 
extrasystoles  were  recorded.  They  were  either  interpolated,  or  followed 
by  a  diastolic  pause  as  long  as  that  after  each  rhythmic  beat.  Four 
years  later,  electrocardiographic  records  of  ventricular  extrasystoles 
were  obtained.  By  derivations  I.  and  II.  their  initial  deflexion  was 
upwards  (Plate  Nil.,  Fig.  33). 

Another  form  of  ventricular  irregularity  was  more  frequently 
encountered.      It  consisted  in  group-beating  of  the  ventricles  with  a 


VA  .r  \ vvui^Ni  \ r 


^yl/#^M\^^ 


RRAfl.    n  fl 


^'•vP-jVAlV 


30,9,09. 


Fig.  42.— Apical  and  brachial  tracings  from  Case  I.,  showing  group-beating  of  the  ventricles. 
The  time  record  is  0-2  second. 

rate  of  41-63  per  minute.  There  were  groups  of  two  to  eleven,  and 
sometimes  about  twenty,  rapid  ventricular  beats  (Fig.  42),  each  group 
terminating  in  a  long  diastolic  pause  of  about  the  same  duration  as 
that  after  a  systole  when  the  ventricles  were  beating  rhythmically 
and  less  frequently.  The  following  figures  represent  inter-ventricular 
periods  in  seconds  and  show  the  group-beating : — 

1-80,  1-00,  0-90,  0-94,  0-86,  0-92,  0-90,  0-97,  0-92,  0*90,  1-76 

1-68,  1-40,  1-00,  0-88,  0-90,  0-92,  0-88,  0-92,  0-92,  0-92,  0-90  .  .  . 

1-76,  1-44,  1-00,  0-92,  0-96,  0-90,  0-95,  0-90,  0-93,  0-96,  0-95,  1-72 

1-76,  1-44,  0-96,  0-95,  0-95,  1-80 

.  .  .  0-94,  0-90,  0-94,  0*90,  0-90,  1-84 

1-86,  1-00,  1-00,  1-24,  1-00,  1-00,  1-24,  1-04,  1-00,  1-30,  1-84. 


CASE   II.  45 

The  diastolic  pause  after  the  first  systole  of  a  group  was  often  longer 
tlian  that  after  the  second ;  this  was  usually  longer  than  that  after  the 
third  and  subsequent  systoles.  There  was  no  lessening  of  the  frequency 
of  the  ventricular  rate  towards  the  end  of  a  group  comparable  to  that 
recorded  by  Wenckebach.^  The  jugulo-carotid  tracings  demonstrated 
that  while  the  ventricles  were  in  group-beating  the  auricles  were  in 
constant,  rapid,  rhythmic  liutter  at  a  rate  of  about  276"9  per  minute. 

The  group-beating  of  tlie  ventricles  was  recorded  electrocardiographi- 
cally  on  many  occasions.  The  ventricular  deflexions  were  not  atypical 
but  on  the  contrary  were  of  the  same  form  as  those  of  the  rhythmic 
series  of  beats  at  a  rate  of  32-36  per  minute.  The  stimuli  for  all  the 
ventricular  beats,  therefore,  were  initiated  at  the  same  site,  namely,  in 
the  main  stem  of  the  atrio-ventricular  bundle  below  the  level  of  the 
severing  lesion.  The  group-beating  of  the  ventricles  in  this  case  is 
evidently  analogous  to  the  series  of  rapid  rhythmic  ventricular  beats 
described  by  Gaskell  ^  as  following  the  application  of  a  single  stimulus 
to  the  auriculo-ventricular  ring  of  muscle,  and  likewise  to  the  group- 
beating  of  the  ventricles  after  the  experimental  production  of  heart- 
block  as  recorded  by  Erlanger  and  Blackman.' 


Case  II. — Auriculak  Fluttee,  at  a  Eate  of  2684-283  per  Minute, 
WHICH  Subsequently  Passed  into  Fibrillation.^ 

A  traveller's  porter,  aged  45  years,  was  admitted  to  the  Eoyal 
Infirmary  on  the  9th  August  1912  complaining  of  shortness  of  breath 
and  of  pain  in  the  left  side  of  the  chest  for  two  months.  Twenty-four 
years  previously  he  had  suffered  from  syphilis,  for  which  he  was  treated 
for  three  months.  Following  the  primary  sore  his  throat  became 
affected,  and  most  of  his  hair  fell  out,  but  he  considered  that  he  had 
been  free  of  any  subsequent  ill  effects.  Four  and  a  half  years  ago  he 
was  confined  to  bed  for  two  months  on  account  of  rheumatic  pains  in 
the  feet  and  legs;  and  two  years  ago  he  met  with  an  accident, 
necessitating  an  amputation  through  the  left  forearm.     He  had  been 

1  "Wenckebach,  K.  F.,  "Beitrjige  zur  Keniituis  der  mensclilichen  Herztatigkeit," 
Arch.  f.  Anat.  ?i.  Fhysiol.  (Physiol.  Abt.),  Leipz.,  1908,  SuppL,  53. 

-  Gaskell,  W.  H.,  "The  Contraction  of  Cardiac  'Mnscle,"  Schdfei-'s  Text-booh  of 
Physiologij,  Edin.  and  Lond.,  1900,  ii.,  179. 

3  Erlanger,  J.,  and  Blackman,  J.  R.,  "Further  Studies  in  the  Phj^siology  of 
Heart-block  in  Mammals.  Chronic  Auriculo-ventricular  Heart-block  in  the  Dog," 
Heart,  Lond.,  1909-10,  i.,  177. 

*  "Auricular  Flutter,"  Edin.  Med.  Journ.,  Edin.,  1912  (X.S.),  ix.,  485. 


46  KECORDS   OF   CASES 

a  moderately  temperate  man.  With  the  exception  of  slight  palpitation 
during  the  past  twelve  months,  he  was  in  good  health  until  eight 
weeks  ago,  when  he  began  to  feel  short  of  breath  on  carrying  his  parcels 
up  flights  of  stairs.  Day  by  day  the  dyspnoea  became  more  pronounced, 
and  he  then  began  to  suffer  from  pain  in  the  left  side  of  the  chest  and 
in  the  epigastric  region.  The  pain  usually  came  on  at  night,  for 
example,  when  he  was  going  upstairs  after  his  day's  work  was  done. 
The  pain  in  the  epigastrium  was  localised  at  an  area  three  inches  below 
the  infra-sternal  notch,  and  this  area  was  tender  on  deep  pressure.  This 
pain  bore  no  relation  to  the  taking  of  food,  but  was  always  aggravated 
when  the  breathing  was  embarrassed,  and  became  less  severe  when  he 
sat  quietly.  He  did  not  complain  of  nocturnal  dyspncea,  he  had  never 
felt  faint  or  lost  consciousness,  and  he  had  never  noticed  any  signs 
of  dropsy. 

On  admission  to  hospital  he  was  a  well-nourished  man,  measuring 
5  feet  8|  inches,  and  weighing  133  lb.  He  was  rather  bald  for  his  years, 
but  presented  no  cyanosis  or  dropsy.  The  chest  was  well  formed.  The 
cardiac  impulse  was  strong  and  unduly  diffuse,  the  apex-beat  being  at 
a  point  in  the  sixth  left  intercostal  space,  four  inches  to  the  left  of  the 
mid-sternal  line.  As  ascertained  by  percussion,  the  right  border  of  the 
heart  lay  IJ  inches  to  the  right  of  the  mid-sternal  line.  Over 
the  mitral  area  a  loud  blowing  systolic  murmur  was  audible.  It  was 
conducted  round  the  left  side  of  the  chest,  and  was  faintly  audible  at 
the  lower  end  of  the  sternum.  A  moderate  degree  of  venous  pulsa- 
tion was  visible  on  the  right  side  of  the  neck.  The  arterial  pulse  was 
at  the  rate  of  138  per  minute,  rhythmic,  and  of  good  force.  The  walls 
of  the  radial  arteries  were  somewhat  thick,  but  the  vessels  were  not 
tortuous.  The  systolic  blood-pressure  was  152  mm.  Hg,  as  ascertained 
by  the  Pdva-Rocci  sphygmomanometer.  He  had  a  slight  cough,  but  no 
expectoration.  The  respiratory  rate  was  28  per  minute.  The  breath 
sounds  were  of  normal  character,  with  a  few  medium  crepitations  and 
rhonchi  at  the  base  of  each  lung.  Neither  the  liver  nor  the  spleen  was 
enlarged.  The  urine  was  somewhat  scanty,  had  a  specific  gravity  of 
1024,  and  contained  a  trace  of  albumin.     No  tube  casts  w^re  detected. 

Progress. — lUh  August. — The  patient  has  been  resting  quietly  in 
bed,  and  taking  10  minims  of  tincture  of  digitalis  with  half  a  grain  of 
sodium  nitrite  thrice  daily  since  his  admission,  and  now  feels  decidedly 
better.  He  passed  70  ounces  of  urine  to-day.  He  still  has  palpita- 
tion, but  no  pain.  The  pulse  has  been  constantly  frequent — 120-140 
per  minute — and  rhythmic.     The  liver  is  now  considerably  enlarged. 


CASE   II. 


47 


extending  clown  to  the  level  of  the  umbilicus  in  the  right  maniniillary 
line.  Electiocauliogianis  recorded  to-day  show  that  the  auricles  are 
beating  rhythmically  at  a  rate  of  28o-0,  while  the  rate  of  the  rhythmic 
ventricular  beats  is  exactly  one-half,  namely,  141-5  per  minute 
(riate  X.,  Fig.  46).     Pressure  on  either  the  right  or  on  the  left  vagus 


Fig.  43. — Auricular  flutter  with  a  ventricular  response  to  every  seconrl  auricular  beat.     The  rate  of  the 
arterial  pulse  is  130'3  per  minute.    Jugulo-carotid  and  brachial  tracings. 

causes  transient  slowing  of  the  ventricles,  but  they  soon  escape  from 
vagus  inhibition  and  resume  their  former  rate  of  contraction, 

Vlth  August. — Polygraphic  records  show  a  ventricular  venous  pulse. 
The  ventricles  usually  contract  rhythmically  at  a  rate  of  136*3  per 
minute,  each  pulse  period  in  the  sphygmogram  being  about  0'44  second 
(Fig.  43).  In  other  parts  of  the  record  there  are  groups  of  three  to  five 
rhythmic  ventricular  beats,  each  inter-systolic  period  measuring  about 


Fig.  44.— Auricular  flutter,  Case  II.  Jugulo-carotid  and  brachial  tracings.  The  ventricles  usually  respond 
to  every  second,  but  occasionally  to  every  third,  auricular  beat.  Grouping  and  alternation  of  the  aiterial 
pulse-beats. 

0*44  sec.  Each  group  of  beats  is  separated  from  that  which  precedes 
or  that  which  follows  it  by  a  period  of  about  0-72-0-80  second,  and  the 
sphygmogram  shows  marked  alternation  of  the  pulse-beats  in  each 
group.  The  first  beat  of  each  group  is  represented  by  a  large  pulse- 
wave  ;  the  second  ventricular  beat  is  rhythmic,  but  the  corresponding 
pulse-wave  is  small,  and  delayed  in  transmission  (Figs.  44  and  45). 

18th  August. — The   patient   slept   ten   hours  last   night,  and   felt 
much  better.     In  electrocardiograms  the  auricular  deflexions  occurred 


48 


EECOEDS   OF   CASES 


rhythmically  at  a  rate  of  280'4  per  minute.  The  ventricles  were 
usually  beating  rhythmically  at  a  rate  of  140'2  per  minute,  in  response 
to  every  second  auricular  stimulus,  but  occasionally  there  was  a  response 
to  every  fourth  auricular  beat.  Pressure  upon  the  right  vagus  caused 
transient  slowing  of  the  ventricles,  while  the  auricular  rate  remained 
unchanged.  The  dose  of  digitalis  tincture  was  increased  to  20  minims 
thrice  daily. 

19^A  August. — The  auricles  were  beating  rhythmically  at  a  rate  of 
276'4  per  minute.  The  ventricular  beats  were  usually  rhythmic  at  a 
rate  of  138-2  per  minute — As  :  Vs  :  :  2  : 1 ;  but  every  now  and  again  the 
ratio  was  4:1,  and  at  these  times  the  auricular  deflexions  were  diphasic. 

2Qth  August. — The  patient  passed  95  ounces  of  urine,  having  a 
specific  gravity  of  1015,  and  still  containing  a  small  amount  of  albumin. 

2'2ncl  August. — He  slept  about  ten  hours  last  night,  has  no  dyspnoea 


Fig.  45,  Case  II. — Tracings  from  the  apex-beat  and  brachial  artery,  shelving  two  groups,  each 
consisting  of  three  rhythmic  ventricular  beats,  and  seven  rhythmic  beats  of  another  group.  The 
groups  are  separated  one  from  another  by  comparatively  long  diastolic  pauses.  The  first 
ventricular  contraction  of  each  group  is  represented  by  a  large  wave  in  the  sphygmogram  ;  the 
second  ventricular  sj'stole  is  represented  by  a  small  wave,  which  is  delayed  in  transmission. 

and  no  dropsy,  and  considers  that  he  would  be  fit  for  his  work  if  he 
were  allowed  to  get  up.  The  sodium  nitrite  was  stopped,  and  the  dose 
of  digitalis  tincture  was  reduced  from  20  to  10  minims  thrice  daily. 
The  auricles  were  beating  rhythmically  276*4  times  per  minute.  The 
ventricles  usually  responded  to  every  fourth  auricular  beat,  but  the 
ventricular  rhythm  was  sometimes  irregular,  there  being  a  response  to 
every  third  or  fourth  auricular  stimulus  (Plate  XV.,  Fig.  82). 

2'drcl  August. — The  radial  pulse  was  rhythmic  at  a  rate  of  72  per 
minute. 

24^/i.  August. — The  arterial  pulse  was  68  per  minute  and  rhythmic. 

2bth  August. — The  pulse  was  rhythmic  at  a  rate  of  72  per  minute. 

2QtJi  August. — The  auricles  were  beating  rhythmically  at  a  rate  of 
268"4;  the  ventricular  beats  were  rhythmic  at  a  rate  of  67"1  per 
minute — a  constant  ratio  of  As  :  Vs  :  :  4 : 1.  The  auricular  deflexions 
were  diphasic. 

27th  August. — Patient  passed  70  ounces  of  urine,  which  was  free  of 


v\j\T\<:  X. 


LUiMMMUnilliailMAUAIIIiyiUiMJAUMMIIMIIMIIIlHIIMUHUHUyAUAiA^ 


Fk:.  4t!.— Aurieuhir  Hiittor  with  a  vontriciUar  response  to  every  second  auricular  beat.     Case  II. 
Derivation  II.    16,  viii.  1912  (see  p.  47). 


lUiiinuiiiiauiuuuiiiiiiutniiiiuitiiiiiiiiiiiiiiiiiitiiiiiiiiitiiuniiiiiiiiuiuiiiiuiuuiuaHiiiiiiiiiauuuitiJiii 


Fk;.  47.— Auricular  flutter  with  a  ventricular  response  to  every  fotntli  auricular  beat.    Case  II. 
Derivation  II.     29,  viii.  1912  (see  p.  49). 


fi.'f^V.^  ; 


iiiuiiiiiiuiiuiiiuaaiHiyiiiiiiiiuiuuuuiiuuiiauuuiiiiiauiiiiiuiiiiiiiuiiiiitiiiiuiiiiuiiiiiiiiiiiiiiitiiiiuiiiiiiuiiuiiii 

Fig.  48.— Auricular  fibrillation.    Case  II.     Derivation  II.     9,  ix.  1912. 
{Ediii.  Meil.  Journ.,  N.S.,  vol.  ix.) 


CASE   II.  49 

all)iuniii.  The  dose  of  digitalis  was  increased  to  15  mininis  tlirice 
daily. 

28^A  AiKjvst. — The  auricles  and  ventricles  were  beating  rhythmically 
at  274-28  and  G8-57  per  minute  respectively,  the  ratio  of  As:A''s:  :4: 1 
being  constant.  The  auricular  deflexions  were  still  diphasic.  Pressure 
upon  the  right  vagus  did  not  retard  the  auricles,  but  caused  transient 
slowing  of  the  ventricles  (Plate  XVIIL).  For  each  pulse-beat  in  the 
sphygmogram  there  were  four  waves  in  the  jugulo-carotid  tracing.  The 
two  waves  occurring  during  ventricular  diastole  were  small.  The  two 
waves  occurring  during  ventricular  systole  were  larger,  and  the  first  of 
them  occurred  immediately  after,  and  was  fused  with,  the  carotid  wave 
(Fig.  49). 

29/!//  August. — The  auricles  and  ventricles  were  beating  at  rates  of 
281-0  and  70-25  respectively,  with  a  constant  ratio  of  As:  Vs:  :4: 1. 


Fig.  49,  Case  II.— Jugulo-carotid  and  bracliial  tracings  recordpd  on  the  2Sth  August  1912.    The 
auricular  and  ventricular  rates  are  2ti6'4  and  06'6  respectively. 

2>Qth  August. — The  dose  of  tincture  of  digitalis  was  increased  to 
20  minims  thrice  daily. 

olst  August. — The  auricles  and  ventricles  were  beating  rhythmically 
at  rates  of  274-28  and  68'57  respectively,  with  a  constant  ratio  of  4:1, 
and  the  auricular  deflexions  were  still  diphasic. 

2nd  September.  — The  patient  was  allowed  up  yesterday  ;  he  slept  for 
nearly  ten  hours  last  night,  and  had  no  pain  or  palpitation.  To-day  he 
was  walking  about  the  ward,  and  felt  quite  well.  The  auricles  and 
ventricles  were  beating  rhythmically  at  rates  of  274-2  and  68-55  respec- 
tively, the  ratio  of  As:Vs:  :4:1  being  constant  except  when  pressure 
upon  the  right  vagus  retarded  the  ventricles,  although  it  exerted  no 
influence  on  the  auricular  rate. 

5t/i  SeiJteniber. — The  arterial  pulse  has  remained  uniformly  rhythmic 
and  its  rate  has  varied  only  from  68  to  72  per  minute.  To-day  the 
auricular  rate  is  274-2,  the  ventricular  68-55  per  minute. 

1th  September. — Electrocardiograms  taken  yesterday  showed  that 
the  ratio  of  As  :  Vs  :  :  4  : 1  was  still  constant.  To-day  the  dose  of  digitalis 
tincture  was  increased  to  30  minims  thrice  daily. 

4 


50 


EECOEDS   OF   CASES 


Wi  Septeniber. — The  patient  felt  well,  and  was  walking  about  the 
ward  and  corridor.  The  arterial  pulse  was  found  to  be  wholly  irregular 
at  a  rate  of  62  per  minute.  Electrocardiograms  (Fig.  48)  revealed 
auricular  fibrillation.  The  auricular  deflexions  were  at  a  rate  of  about 
467  per  minute.  They  were  not  uniformly  rhythmic,  and  were  no 
longer  diphasic. 

IQth  Septeviber. — The  ventricles  were  beating  wholly  irregularly  at 
a  rate  of  about  60  per  minute.  Electrocardiograms  showed  small 
irregular  auricular  deflexions  at  a  rate  of  about  457  to  500  per  minute. 
Many  of  the  ventricular  beats  were  represented  by  atypical  deflexions. 
[None  of  these  atypical  beats  were  premature ;  on  the  contrary,  each 
was  preceded  by  a  long  diastolic  pause.     In  one  part  of  the  record  three 


Fig.  50. — Orthodiagram  of  heart  and  aorta 
at  end  of  tranquil  Inspiration.     Case  II. 

atypical  beats  occurred  in  series.  The  digitalis  was  stopped — he  had 
taken  1575  minims  in  the  course  of  32  days.  An  orthodiagram 
(Fig.  50)  showed  that  all  the  diameters  of  the  heart  were  considerably 
enlarged ;  the  long  diameter  from  the  cavo-auricular  junction  to  the 
apex  was  18-3  cm.;  the  curves  of  the  right  auricle  and  left  ventricle 
extended  outwards  6  and  9  cm.  respectively  from  the  mesial  line.  The 
left  auricular  curve  was  absent ;  the  pulmonary  and  aortic  curves  on 
the  left  side  were  somewhat  more  prominent  than  normal. 

llth  Septemher. — The  auricles  were  still  in  fibrillation.     In  electro- 
cardiograms the  rate   of  the   auricular   deflexions  was  about  476  per  ■ 
minute;  the  ventricular  rate  was   about   65   per  minute,   with  inter- 
systolic  periods  of  0-73,   0-99,  1-29,   1-22,  0-85,  0-67,  0-84,  0-91,  0-64, 
€'71,  1"01  second. 

14^;^  Septemher. — The  rhythm  of  the  ventricles  has  remained  wholly 


CASE   in.  51 

irregular.  Electroeardiograins  recorded  on  tlie  12th  and  again  to-day 
showed  auricuhir  librillation. 

15th  Scptemher. — The  ventricles  were  still  irregular  at  a  rate  of 
70  per  minute.  The  niaxiniuni  systolic  pressure  was  140,  the  diastolic 
pressure  90  nnn.  Hg. 

16//t  Scptoiiher. — Continuous  irregularity  of  the  ventricles — the 
rate  was  80  per  minute.  Administration  of  mercury  and  iodide  was 
commenced. 

19th  September. — The  pulse  was  wholly  irregular,  with  a  rate  of 
88  per  minute. 

About  a  fortnight  later  the  patient  was  not  so  well ;  the  pulse-rate 
had  become  more  frequent,  the  administration  of  mercury  and  iodide 
was  stopped,  and  digitalis  was  again  administered.  On  the  22nd 
October,  the  last  occasion  on  which  the  patient  was  seen,  the  auricles 
were  still  in  fibrillation. 

Case  III. — Aukicular  Fluttee  at  a  Bate  of  320  per  Minute; 
Onset  of  Fibrillation  under  the  Influence  of  Strophan- 
thin;  Subsequent  Eeturn  to  Physiological  Rhythm;  Death 
Ten  Days  after  the  Flutter.^ 

A  cabman,  aged  37,  married,  but  without  children,  was  admitted  to 
the  Royal  Infirmary  on  the  25th  February  1912,  under  the  care  of  the 
late  Dr.  George  A.  Gibson.  The  patient  was  complaining  of  swelling 
of  the  abdomen,  and  of  an  uncomfortable  feeling  after  taking  food.  He 
had  suffered  from  acute  rheumatism  three  times — when  15,  22,  and  27 
years  of  age — but  denied  having  suffered  from  venereal  disease.  He 
was  a  moderate  drinker.  For  about  six  weeks  he  had  been  complaining 
of  shortness  of  breath,  especially  on  exertion,  but  he  had  not  experienced 
any  pain,  palpitation,  or  faintness.  On  admission  he  was  listless  and 
markedly  cyanotic,  but  not  dropsical.  He  was  5  feet  0|  inches  in 
height,  and  weighed  137  lb.  The  heart  was  enlarged,  the  apex-beat 
being  in  the  sixth  left  intercostal  space,  4|  inches  from  the  mid-sternal 
line.  A  loud  systolic  and  a  softer  diastolic  mitral  murmur  were  con- 
stantly audible ;  a  rough  presystolic  mitral  murmur  could  usually  be 
heard,  but  it  was  not  constant.  The  arterial  pulse  was  rhythmic  and 
not  unduly  frequent,  the  walls  of  the  radial  arteries  were  not  palpably 
thickened,  and  the  maximum  systolic  pressure  did  not  exceed  110  mm. 
Hg.     Electrocardiograms  recorded  on  the  28th  February  and  on  the 

1  "Auricular  Flutter,"  Edin.  Med.  Joum.,  Edin.,  1912  (X.S.),  ix.,  485. 


52  EECOEDS    OF   CASES 

7th  March  1912  showed  that  each  auricular  beat  was  followed  by  a 
ventricular  contraction.  The  auricular  and  ventricular  deflexions  were 
similar  to  those  in  Plate  XI.,  Figs.  56,  57,  and  58.  The  patient  was 
treated  with  strychnine  and  digitalis,  and  was  discharged  on  the  28th 
March  1912  much  improved. 

He  was  re-admitted  on  the  21st  July  1912  under  the  care  of  Professor 
Wyllie.  The  patient  was  then  complaining  of  shortness  of  breath  and 
swelling  of  the  feet  and  ankles.  He  sometimes  had  palpitation  at  night, 
but  had  not  suffered  any  pain.  On  several  occasions  he  had  felt  faint, 
and  had  to  grasp  a  railing  to  steady  himself. 

The  apex-beat  was  situated  5^  inches  to  the  left  of  the  mid-sternal 
line.  Considerable  pulsation  was  visible,  both  in  the  epigastrium  and 
in  the  jugular  veins  on  the  right  side  of  the  neck.  The  same  mitral 
murmurs  were  audible  as  when  the  patient  was  in  hospital  previously. 
The  arterial  pulse  was  rhythmic,  and  its  rate  was  94  per  minute. 
Examination  of  the  lungs  revealed  no  abnormality ;  the  urine  was 
scanty  and  contained  albumin. 

To  Professor  Wyllie's  resident  physician,  Dr.  J.  M.  Murray,  I  am 
indebted  for  the  following  clinical  notes  of  the  patient's  progress : — 
He  was  given  a  milk  diet,  and  5  minims  of  tincture  of  strophanthus 
and  10  grains  of  potassium  citrate  were  administered  thrice  daily.  On 
the  23rd  July  he  began  to  take  10  grains  of  diuretin  thrice  daily.  On 
the  24th  July  the  patient  was  feeling  better.  He  passed  148  ounces  of 
urine,  and  the  oedema  had  lessened.  His  pulse-rate  had  varied  from 
84-96  per  minute.  On  the  26th  July  there  was  some  sickness,  and 
tincture  of  digitalis  in  5-minim  doses  thrice  daily  was  substituted  for 
strophanthus.  The  rate  of  the  pulse  was  88,  and  its  rhythm  was 
regular. 

On  the  31st  July  the  pulse  was  at  a  rate  of  76,  and  regular.  The 
patient  felt  very  well.  The  oedema  had  disappeared  and  the  digitalis 
was  stopped.  By  the  9th  August  he  had  improved  steadily  and  was 
feeling  very  well,  but  he  was  still  kept  in  bed,  and  he  continued  to  take 
potassium  citrate  and  diuretin.  His  pulse-rate  varied  from  68-72  per 
minute.  On  15th  August  he  was  allowed  to  get  up  for  a  short  time. 
The  pulse-rate  had  been  68-72  per  minute.  On  the  17th  and  18th  he 
was  feverish  (temperature  lOO-O""  F.).  On  the  20th  August  the  legs 
were  again  cedematous ;  his  pulse-rate  had  been  about  80-98  per 
minute,  and  he  was  again  confined  to  bed.  On  the  1st  September  his 
pulse-rate  was  92-98,  and  he  commenced  to  take  10  minims  of  tincture 
of  digitalis  thrice  daily. 


CASE   III.  53 

On  the  7th  September  the  patient's  condition  was  decidedly  worse, 
and  hardly  any  pulse  could  be  felt  at  the  wrist.  On  the  following  day 
liis  condition  was  much  the  same. 

On  the  9th  September  his  arterial  pulse-rate  was  IGO  per  minute; 
the  beats  were  rhythmic  and  equal,  but  of  small  volume.  Marked 
pulsation  was  seen  in  the  jugular  veins,  and  tracings  taken  at  1.15  p.m. 
revealed  a  ventricular  venous  pulse  (Fig.  51).  He  vomited  once  early 
in  the  afternoon.  Electrocardiograms  (Plate  XI.,  Figs.  52,  53,  and  54) 
taken  at  3  o'clock  showed  that  the  auricles  were  beating  rhythmically 
at  a  rate  of  320,  while  the  ventricular  beats  were  rhythmic  at  a  rate 
of  160  per  minute.  From  5.28  until  5.30  p.m.  the  ventricular  rate, 
estimated  from  a  venous  pulse  tracing,  was  constantly  162*1  per  minute. 
At  5.31  P.M.  O'OOl  gramme  of  strophanthin  (Boehringer)  was  given 
intravenously,  and  a  polygraphic  record  was  taken  every  minute  until 

0-2  see. 

Fig.  51,  Case  III.— Jugulo-carotid  and  brachial  tracings.    The  arterial  pulse-rate  is  lo9-5  per  minute. 
The  .jugular  pulse  is  of  the  ventricular  form. 

6.1  P.M.  This  record  showed  that  the  ventricular  rate  fell  to  155-2  at 
5.33,  varied  from  153*8  to  16'2*1  until  5.41,  and  remained  constant  at 
157*9  from  5.42  until  5.59.  At  6  p.m.  the  rate  was  162*1,  and  at  6.1, 
half  an  hour  after  the  injection,  the  rate  was  161*3.  At  6.3  p.m.  pressure 
upon  the  right  vagus  retarded  the  ventricles  for  a  few  seconds,  after 
which  they  resumed  their  former  rate.  At  8  p.:m.  the  arterial  pulse  had 
fallen  to  128  per  minute,  and  its  rhythm  was  irregular.  He  vomited 
several  times  during  the  evening,  and  complained  of  some  pain  in  the 
muscles  of  the  arm  into  w^hich  the  injection  had  been  given.  He  slept 
poorly. 

On  the  following  day  (10th  September)  he  felt  better,  though  still 
troubled  with  cough  and  dyspnoea.  The  lungs  presented  no  signs  of 
oedema.  The  arterial  pulse  was  less  frequent  (96-104  per  minute)  and 
of  larger  volume,  but  it  was  wholly  irregular  for  the  first  time.  An 
electrocardiogram  (Fig.  55)  showed  both  the  disorderly  action  of  the 
ventricles  and  the  small  irregular  quick  deflexions  characteristic  of 
auricular  fibrillation.     The  auricular  deflexions  were  at  a  rate  of  about 


54  EECORDS   OF   CASES 

400  per  minute.  The  dose  of  tincture  of  digitalis  was  increased  to 
15  minims  thrice  daily. 

On  the  succeeding  day  (11th  September)  he  looked  and  felt 
decidedly  better.  He  had  slept  well  and  the  feet  had  become  less 
oedematous.  The  arterial  pulse  was  perfectly  rhythmic  at  a  rate  of 
about  90  per  minute.  Electrocardiograms,  recorded  by  derivations  I., 
II.,  and  III.,  showed  that  each  auricular  beat  was  followed  by  a 
ventricular  contraction,  and  that  the  As—  Vs  interval  was  0*15  second 
(Eigs.  56,  57,  and  58).  In  these  electrocardiograms  the  auricular  and 
the  ventricular  deflexions  were  of  the  same  form  as  those  in  the 
records  taken  six  months  previously ;  but  on  comparing  the  auricular 
deflexions  when  the  auricles  were  in  flutter  (Figs.  52,  53,  and  54)  with 
those  when  they  were  beating  slowly  (Figs.  56,  57,  and  58)  it  is  evident 
that  the  former,  especially  as  recorded  by  derivations  I.  and  III.,  were 
of  abnormal  form.  When  the  auricles  were  in  flutter,  the  stimulus 
for  each  contraction  was  therefore  initiated  at  an  abnormal  site. 

On  the  13th  September  he  remained  fairly  well,  and  his  pulse  was 
rhythmic  at  a  rate  of  98  per  minute.  On  the  14th  and  15th  he  was 
obviously  worse,  his  face  having  an  icteric  tint.  His  pulse  was  90-100, 
and  rhythmic.  In  electrocardiograms  recorded  on  the  14th,  each  auri- 
cular beat  w^as  seen  to  be  followed  by  a  ventricular  contraction.  On 
the  16th  the  right  knee  became  swollen  and  painful.  He  was  given 
aspirin  thrice  daily,  and  on  the  17th  the  joint  had  improved.  His 
pulse  was  rhythmic  at  a  rate  of  100-102  per  minute.  On  the  18th 
the  pulse  was  still  rhythmic,  and  at  a  rate  of  88-96 ;  the  dose  of  digi- 
talis tincture  was  reduced  to  5  minims  thrice  daily.  On  the  same 
evening,  however,  he  was  suddenly  seized  with  severe  breathlessness. 
Examination  of  the  chest  revealed  evidence  of  a  pleural  effusion.  After 
25  ounces  of  fluid  had  been  withdrawn  he  was  somewhat  relieved  for  a 
time,  but  the  dyspnoea  soon  recurred.  It  was  not  relieved  by  xw  grain 
of  strophanthin  given  subcutaneously,  and  the  patient  died  on  the 
following  morning. 

The  pathological  appearances  of  this  heart  have  been  described 
on  p.  30. 

Case  1\. — Auriculae  Fluttee  at  a  Rate  of  256-270  pee  Minute 

IN    AN    OTHERWISE    HEALTH Y   HEAET  ;    EeCOVERY.^ 

A  railway  clerk,  aged  21,  had  enlarged  glands  and  sinuses  in  the 
neck  since  he  was  seven  years  old,  but  otherwise  had  enjoyed  good 

1  "  Aiiricular  Flutter,"  Edin.  Med.  Journ.,  1912  (X.S.),  ix.,  485. 


PLATK    Xl. 


rv, 

■•If   ^^MMftF    ^0ti0tw    ^^•••f    f^^i^tw    ^I^^^W^    r^^^tmt'   ^0mt00    MNnRHF   ^ 


iiliiiiiiinniiiiiiuii  wiiiiinniiiiii  1 1 1 1  iii  1 1 1 1  n  i  Miiiiiiniiiiiiiniinii  n  1 1 1 1 1 1 1  iim 
Fig.  .')!>. — Auiicular  llutliT.     DciiviiliDii  1.     '.i,  ix.  I'.ilJ. 


ys\/^^ \p>^^^^»m^  ^S^>yS  ^-WN  fS0^  f^^  fS^  f\ 

s 
iiiiiiiiiiiiiiiiiiiiiiii 1 1  III  1 1 1 1 1 1 1  iiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiii,,, 

Fu;.  -I'i. — Auiiciilar  MuttiT.     Deri v;it ion  11.    '.',  ix.  I'.il'J. 


I  I  I  I 


V       T      V       F        P        T         P 

«^ /*-^  A-^ /^ /^ /-^  A-^  A^  A<^  A- 

Q  S 

II I  1 1  It  1 1 1 1 1 1 1 1 1 1 1 1 11 1  It  II 11  I  I  1 1 i 1  I  I  II  1 1 11 II 1 1 1 1  I  I  I  II  i 1 1  I  I  I  II  i  I  1  1  I  1  I W 1 1  1 1 1 1  II I  I  I  1 1 1 1 1  1 1 1 II  1 1  II  I 
Pig.  5i. — Auricular  flutter.     Derivation  III.     '■>,  ix.  lulJ. 


o 

llllllimilllUlllillHIIIIIIIIIIIIIIIIIIIIlMIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIUIIiilillllllllilllllllllllllllllilMIIIIIIIIIIIHIIUIillllMIIIH  

Fig.  55. — Auricular  fibrillation.     Derivation  II.     10,  ix.  l;il2.     Nineteen  hours  after 
stroplianthin  intravenously. 


1   p  ^ 

w\  /i*%^i^'  F«^w\'  P^^'tg^  ;w«*H*«»*w'  fa«W^'  ^^^^  /«»**W  P* 

\  \  ',  \  \  >•  i  ^ 

s 
.iiiiiiiiiiiiiiiiiiiiiiiiiuiiiiiiiuuiiiiuiuiuiiiiiiiiiiiiiiiiiiiiiituiuuituuuuiiiiiuiiuiiiiumtiiiuiiiuiuiunuim^^^^^^ 

Fig.  50. —Normal  rhvtlini.     Derivation  I.     1'2.  ix.  V.H2. 


»  pi  I 


'^  M00mm\  JiimiJ\  ^,>^^^ 


IlllllllllllllllllUlllllllllllllllllllilllllllllllll'IIIIIIIIIUIIIIIII 


•^  ^t****^  m^'"*^^  iM^**^  yi«<« 

I  Q 

lUiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiuiiiiiiiiiiiniiiiiiiiiiiiiiiiti 


Fic.  57.— Normal  rhvthm.     Derivation  II.  Fig.  5S. — Normal  rhythm.     Derivation  III. 

11,  ix.  1012.  11,  ix.  1!)12. 

Electrocardiograms  from  Case  III.  In  Fig.  55  the  tension  of  the  string  was  adjusted  so  as  to  give  a 
deflexion  of  1 '5  em.  for  1  millivolt.  In  the  remaining  records  1  cm.  =  l  millivolt.  The  time  record  is  2S'57 
per  second.     (Ediii.  Med.  ■Journ.,  N.S.,  vol.  ix.) 


I'LATK   Xir. 


?i    ft 


p  Tpy 


6'         /3 


5         S 


Fill.  59.— Atiiicular  lluttcr.     C:is(nV.     Derivation  1 1.     Ion.-]  iiiilli\'ijlt. 
(lidln.  Akd.  Journ.,  N.S.,  ^■ol.  ix.) 


^i 


^iAmA^^^m 


I  j  I 


iiiuiiutiiiiiiiiiiiiiiiiiiiiuiaiutii        iiiiiuiuiMiHiiiyiUHiHtiiiiuiiiUiyu        iiiijiuiiitiiitiiitiniiiiiuiiiiiiiiiiiitiiiiii 

Figs.  00,  01,  &2. — Electrocaidiograms  by  derivations  I.,  II.,  and  III.,  after  restoration  of  tlie  normal 
riiytlim  in  Case  IV.     1  cm.  =1  millivolt. 


Fig.  63. — Auricular  flutter  at  a  rate  of  285-6  per  minute.  The  ventricles  are  responding  rhythmically 
at  a  rate  of  142 -S  per  minute.  The  auricular  deflexions  are  alternatelyjnerged  in  2',  and  precede 
iJ  by  0-07  second.     Case  XI.    Derivation  II.     1  cm.  =  1  millivolt. 


■p       p       -p        -p       -p        T        T        T 


iiiitiuiiiiiiiitiiuiiiitiiiiiiuiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiimiiiiuiiiiiiiiiiiiiiiiiiaiiiiiiiiiiiiii 

Fk;.  H4.— Auricular  flutter.      Case  XI.     The  rate  per  minute  of  the  auricles  is  2S;3-0,  while  that  of  the  ventricles 
is  1-!2'S.     Derivation  III.     1  cm.  =  1  millivolt. 


CASE   IV.  55 

health,  and  had  never  suffered  from  acute  rheumatism,  chorea,  scarlatina, 
or  sypliiiis.  In  May  1911  he  suffered  from  palpitation  for  two  or 
three  weeks  wlienever  he  exerted  himself.  He  could  then  feel  his 
heart  beating  forcibly  and  at  a  great  rate.  The  attack  of  palpitation 
might  pass  oft"  in  a  few  minutes,  or  might  persist  for  two  or  three 
days,  and  would  then  prevent  him  from  sleeping.  In  November  1911 
the  palpitation  recurred,  and  was  associated  with  vertigo,  which  was 
even  more  troublesome.  Both  symptoms  used  to  appear  whenever  he 
underwent  any  unusual  exertion;  for  example,  when  he  ran  upstairs,  or 
after  a  wrestling  bout,  but  at  all  other  times  he  felt  perfectly  well.  On 
one  occasion,  after  running,  he  nearly  fainted.  He  never  experienced 
any  pain  or  dyspna?a.  He  had  been  off  work  for  fourteen  weeks  when 
he  was  admitted  to  the  Eoyal  Infirmary  under  the  care  of  Professor 
Faissell  in  May  1912. 

Electrocardiograms  taken  on  the  10th  May  1912  showed  that  the 
ventricles  were  beating  irregularly  in  response  to  supra-ventricular 
stimuli.  The  ventricular  periods  estimated  from  an  electrocardiogram 
were  0-45,  042,  0-35,  0-77,  0-43,  0*49,  0-45,  0-45,  0-49,  0-39,  0-49,  0-35, 
0-45, 0-80, 0-42, 0-49,  0-45,  0-43,  0*45,  0-49,  0-42, 0-35  second.  These  figures 
indicate  that  the  ventricles  were  usually  beating  at  a  rate  of  about 
122-133  per  minute,  and  that  there  was  a  comparatively  long  diastolic 
pause  after  a  group  of  several  frequent  beats.  The  ventricular 
arrhythmia  is  illustrated  in  Fig.  59,  where  each  of  the  longer  pauses 
is  approximately  equal  to  the  sum  of  the  two  antecedent  ventricular 
periods.  The  auricular  rhythm  was  also  irregular.  There  were  series 
of  8-10  auricular  beats  occurring  wholly  or  almost  rhythmically  at  a 
rate  of  256-270  per  minute,  and  terminating  in  a  diastolic  pause  of 
about  0*7  second  duration  (Fig.  59).  The  irregularity  of  the  ventricles 
was  due  in  part  to  the  auricular  irregularity,  and  more  especially  to  the 
occurrence  of  a  comparatively  long  auricular  diastole  every  now  and 
again.  The  ventricular  irregularity,  however,  was  also  due  to  the  fact 
that  even  when  the  auricles  were  beating  fairly  rhythmically  successive 
ventricular  contractions  occurred  in  response  to  a  varying  number  (for 
example,  4,  2,  3,  2,  etc.)  of  auricular  beats.  The  auricular  flutter  was 
not  arrested  by  pressure  on  the  right  A'agus. 

The  patient  stayed  in  hospital  for  five  weeks,  and  a  fortnight  after 
his  return  home  he  was  able  to  resume  his  work.  "When  he  was 
again  examined  four  months  later,  he  was  still  feeling  perfectly  well. 
His  heart  was  of  normal  size,  without  any  sign  of  a  valvular  lesion,  and 
the  rhythm  was  a  physiological  one  (Plate  XII.,  Figs.  60,  61,  and  62). 


56  EECOEDS   OF   CASES 

The  flutter  in  this  case  differs  from  that  in  most  other  recorded 
cases  in  not  being  continuous,  but,  on  the  contrary,  intermittent ;  and 
further,  the  auricular  deflexions  during  the  flutter  were  monophasic 
and  of  the  same  form  as  when  the  beats  were  physiological. 

Case  V. — Tkansitions  between  Auriculae  Flutter,  Fibrillation, 
AND  A  Combined  Form  of  Auricular  Activity.^ 

The  patient,  a  miner,  aged  38,  was  a  married  man  with  four 
healthy  children.  His  only  antecedent  illness  was  an  attack  of  acute 
rheumatism,  lasting  for  four  months,  twelve  years  previously.  At 
times  he  had  been  immoderate  in  the  use  of  alcohol.  For  three  weeks 
before  his  admission  to  hospital  he  had  experienced  shortness  of  breath, 
pain  at  the  lower  part  of  the  sternal  region,  and  a  choking  sensation 
in  the  same  region,  "as  if  a  lump  wei^e  there  which  he  could 
not  swallow."  The  act  of  deglutition,  however,  was  not  attended  by 
any  difficulty  or  pain,  and  his  appetite  was  good.  He  had  not  suffered 
from  palpitation  or  faintness,  nor  had  there  been  any  dropsy. 

On  admission  to  the  Eoyal  Infirmary  under  the  care  of  Professor 
Eussell,  the  patient  was  found  to  be  a  rather  poorly-nourished  man 
of  5  feet  7  inches,  weighing  143  lb.  His  complexion  w^as  pale,  and 
although  the  ears  and  nose  were  of  a  red  tint  there  was  no  cyanosis. 
The  cardiac  impulse  was  widespread,  forcible,  and  usually  irregular, 
the  point  of  maximum  impulse  being  in  the  sixth  left  intercostal  space 
4  inches  from  the  mid-sternal  line.  The  only  endocardial  murmur 
was  a  rough  diastolic  murmur,  of  mitral  origin,  which  became  audible 
during  the  longer  ventricular  pauses.  The  walls  of  the  radial  and 
brachial  arteries  presented  a  moderate  degree  of  diffuse  thickening,  and 
the  systolic  arterial  pressure  was  equal  to  140  mm.  Hg.  The  lungs, 
abdomen,  urine,  and  nervous  system  presented  no  abnormal  features. 

During  the  first  four  days  the  patient  was  in  hospital  his  ventricular 
action,  although  sometimes  rhythmic,  was  usually  irregular,  and  was 
constantly  accelerated.  When  the  ventricles  were  beating  rhythmically 
the  auricles  were  in  flutter,  there  being  a  ratio  of  As  :  Vs  :  :  2  : 1.  When 
the  ventricles  were  irregular  the  auricles  were  either  in  fibrillation 
or  in  a  form  of  activity  indicating  flutter  combined  with  fibrillation. 
During  his  stay  in  hospital  the  patient  took  fourteen  I^Tativelle's 
granules,  each  containing  tt}-^  grain  of  digitaline.     In  the  course  of  a 

1  "Further  Observations  on  Auricular  Flatter,"  Quart.  Journ.  of  Med.,  Oxford, 
1913-14,  vii,,  1. 


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CASE   V.  57 

few  days  he  obtained  entire  relief  from  all  his  symptoms,  and  on  the 
eighteentli  day,  when  his  pulse  was  still  irregular  and  accelerated,  and 
when  he  was  still  taking  one  granule  daily,  he  felt  perfectly  well  and 
insisted  on  returning  home.  Thus  no  opportunity  was  afforded  of 
observing  the  nature  of  the  auricular  action  after  the  digitaline  was 
discontinued. 

1.  I'he  Aiiriclcs. — Three  forms  of  auricular  action  were  observed — 
flutter,  fibrillation,  and  a  combined  form, 

(a)  Flutter  was  recorded  by  derivations  II.  and  III.  By  both 
derivations  the  auricular  deflexions  were  rhythmic,  of  large  amplitude 
(200  microvolts),  of  constant  form  except  when  distorted  by  ventricular 
deflexions,  and  usually  occurred  at  a  rate  of  339-343  per  minute.  On 
one  occasion,  immediately  after  the  auricles  had  passed  from  fibrillation 
into  flutter,  the  auricular  rate  was  as  high  as  377'2  per  minute. 

When  the  ratio  of  As :  Vs  was  2  : 1  the  auricular  deflexions  were 
distorted  by  those  of  ventricular  origin,  and  thus  the  true  nature  of 
the  heart's  action  was  somewhat  obscured.  The  auricular  flutter  was 
revealed  clearly,  however,  when  the  ventricles  were  retarded  by  means 
of  pressure  on  the  right  vagus  in  the  neck.  This  is  illustrated  in  Plate 
XIII.  The  record  starts  with  fifteen  rhythmic  ventricular  beats  at  a  rate 
of  169*7  per  minute.  The  corresponding  beats  of  the  brachial  pulse  are 
hyperdicrotic  but  not  alternating.  The  auricular  rate,  meanwhile,  is 
exactly  twice  that  of  the  ventricles,  namely,  339'4  per  minute.  The 
summits  of  successive  F  deflexions  fall  0"10  second  after  the  commence- 
ment of  F  and  synchronously  with  the  summit  of  T  respectively. 
Pressure  upon  the  right  vagus  slows  the  ventricles  markedly.  The 
longer  of  the  two  prolonged  ventricular  diastoles  lasts  for  1"75  second. 
While  the  ventricles  are  retarded  the  auricular  deflexions  continue 
rhythmically  at  a  rate  of  342"8  per  minute. 

The  initial  auricular  deflexion  is  upwards ;  there  are  two  summits, 
of  which  the  second  is  the  higher.  The  curve  then  descends  below,  and 
subsequently  regains,  the  level  at  which  Q  starts,  but  the  diphasic  form 
of  the  auricular  deflexions  is  less  obvious  than  in  Cases  I,  and  II, 

(b)  Fibrillation. — The  auricular  deilexions,  as  a  rule,  occurred  at 
a  rate  of  about  415-467  per  minute.  They  were  either  small  and 
markedly  irregular  in  form  and  rhythm  (fine  fibrillation)  or  larger 
(50-150  microvolts)  and  less  irregular  in  form  and  rhythm  (coarse 
fibrillation)  (Plate  XXL,  Fig,  106), 

(c)  The  simultancoiis  occurrence  of  jiutter  and  Jibrillation  was 
characterised   by  auricular    deflexions    at    a    rate    of    about    367    per 


58,  EECORDS   OF   CASES 

minute,  of  fairly  constant  but  not  diphasic  form,  of  considerable 
amplitude  (about  150  microvolts),  and  almost  wholly  rhythmic. 
Between  this  form  and  coarse  fibrillation  on  the  one  hand  and 
flutter  on  the  other  there  were  no  hard-and-fast  lines  of  distinction. 
2.  The  Ventricles. — When  the  auricles  were  fluttering  the  ventricles 
beat  rhythmically  at  a  rate  of  169 '7- 171  "6  per  minute,  the  auriculo- 
ventricular  ratio  being  constantly  2  : 1.  The  arterial  pulse  was  small 
and  hyperdicrotic,  as  in  the  first  portion  of  Fig.  65,  but  it  was  never 
alternating.  On  one  occasion,  immediately  after  the  cessation  of 
auricular  fibrillation,  a  ventricular  rate  of  188'6,  with  an  auricular 
rate  of  377"2  per  minute,  was  recorded  (Plate  XXL).  When  the  auricles 
were  in  fibrillation  the  ventricular  contractions  were  arrhythmic  and 
less  frequent,  their  rate  varying  from  76  to  107'1  per  minute.  When 
the  auricular  action  was  a  combination  of  flutter  and  fibrillation  the 
ventricular  rhythm  was,  in  the  main,  wholly  irregular,  but  occasionally 
the  length  of  some  of  the  inter-ventricular  periods  was  an  exact  multiple 
of  the  average  P-P  interval,  suggesting  that  a  regular  auricular  rhythm 
predominated  now  and  then.  Thus  in  one  record,  where  the  average 
P-P  interval  was  about  0"14  second,  the  inter- ventricular  periods  were — 

0-59,  0-42,  0-69,  0-89,  0-80,  0-70,  0-42,  0-42,  0-45,  1-12,  0-98,  0-45,  sec. 
=  0-14x    3  5        3        3  8        7 

In  another  record  the  rate  of  the  auricular  deflexions  was  about  367'1 
per  minute,  and  the  inter- ventricular  periods  were — 
0-63,    0-64,    0-73,    0-94,    0-60,    0-63,    0-87,    0-45,    0-91,    0-63  second. 

^  2-0~  2^10  1^99 

The  grouping  of  the  beats  is  almost  exactly  constant,  which  suggests 
that  there  is  a  regular  dominant  rhythm  of  the  auricles. 

Case  VI. — Aupjcular  Flutter  at  a  Rate  of  333-340  per  Minute  ; 
Subsequent  Onset  of  Auricular  Fibrillation  which  Persisted 
UNTIL  A  Fortnight  before  the  Patient's  Death.^ 

The  patient,  aged  59,  had  no  antecedent  history  of  acute  rheumatism 
or  valvular  disease,  but  for  several  years  he  had  been  subject  to 
paroxysmal  attacks  of  tachycardia  in  which  the  ventricles  beat  irregu- 
larly at  a  rate  of  about  158  per  minute;  and  there  had  been  a 
syncopal  seizure  on  one  occasion.  From  each  of  these  attacks  the 
patient   had  made  a  rapid  and   speedy  recovery  after  the  heart   had 

1  See  also  Mackenzie,  Diseases  of  the  Heart,  third  edition,  Lond.,  1913,  Appendix, 
Case  63. 


CASE  VI. 


59 


regained  its  normal  rhythm.  The  last  attack  of  flutter  began  five 
months  before  the  patient's  death.  Dyspnoea,  palpitation,  Cheyne- 
Stokes  breathing  and  insomnia,  were  the  dominant  symptoms.  The 
auricles  were  beating  rhythmically  at  a  rate  of  333-340  per  minute. 
The  auricular  waves  in  the  jugular  veins  were  of  large  size  (Fig.  66). 
Meanwhile  the  ventricular  rate  was  about  110  per  minute,  and  the 
rhythm  was  notably  irregular,    for  although  the  auriculo-ventricular 


^     « A      A  ^  a     f^  \     aa.    a        a.        f    .^    a  '^ 


Fic.  Oi;.— Auricular  flutter  at  a  rate  of  300  per  minute.    Tlie  ventricular  responses  to  every  third  aiu'icular 
beat  are  of  unequal  strength.    Case  VI. ,  jugulo-carotid  and  brachial  tracings. 

ratio  was  often  3:1,  it  frequently  varied  between  2:1,  3:1,  and  4:1. 
The  ventricles  could  not  be  retarded  by  compression  of  the  vagus  on 
either  side. 

The  symptoms  of  cardiac  failure  becoming  more  urgent,  the  daily 
dose  of  digitalis  tincture  was  increased  to  1  drachm.  Four  days  later, 
the  large  auricular  waves  disappeared  from  the  jugular  veins,  the  venous 
pulse   acquired   the   ventricular  form,  and  the  arterial  pulse    became 


Fig.  f)V.— Jugulo-carotid  and  brachial  tracings  from  Case  VI.,  after  development  of  auricular  tibrillation. 

wholly  irregular  (Fig.  67).  The  auricular  flutter  had  apparently  passed 
into  fibrillation.  Subsequently  the  ventricles  became  dilated,  the  mitral 
valve  incompetent,  and  the  urine  scanty  and  albuminous.  The  auricles 
apparently  remained  in  fibrillation  for  three  and  a  half  months.  There- 
after, during  the  fortnight  preceding  the  fatal  issue  and  while  the 
administration  of  digitalis  was  still  being  continued,  periods  of  auricular 
fibrillation,  with  ventricular  arrhythmia,  alternated  with  others  in 
which  the  venticles  were  beating  rhythmically  at  a  rate  of  64-80  per 
minute. 


60  EECOEDS   OF   CASES 

Case  VII.  —  Exophthalmic  Goitee  ;  Extrasystolic  Arrhythmia  ; 
Probable  Onset  of  Auricular  Flutter  ;  Terminal  Auricular 
Fibrillation;  Degenerative  and  Inflammatory  Changes  in 
THE  Auricular  Musculature. 

Mrs.  H.,  aged  41  years,  suffering  from  exophthalmic  goitre,  was 
under  my  care  in  the  Eoyal  Infirmary  in  1911.  The  thyroid  had 
been  enlarged  for  fourteen  years.  Seven  weeks  before  her  admission 
to  hospital,  exophthalmos,  tachycardia,  nervousness,  and  emaciation 
became  pronounced.  There  was  brown  pigmentation  of  the  skin, 
particularly  of  the  abdomen.  The  heart  was  dilated  and  feeble.  The 
ventricular  rate  was  usually  about  100  per  minute. 

For  some  days  after  her  admission  to  hospital,  records  showed 
occasional  extrasystoles    which   were   certainly   supra-ventricular,  and 


Pig.  68.— Sinus  irregularity  and  two  extrasystoles  (third  and  eighth  beats).    Jugulo-earotid  and  brachial 

tracings  from  Case  VII. 

probably  auricular,  in  origin.     The  inter-systolic  periods  in  a  tracing 
from  the  apex-beat  were — 
0-60,    0-60,    0-40,    0-75,    0-64,    040,    0-70,    0-65,    0-60,    0-60  second. 


1-20  1-15  1-10  1-20 

These  figures  indicate  that  the  post-extrasystolic  pause  was  not  fully 
compensatory  and  that  the  second  beat  after  each  extrasystole  had 
a  longer  diastolic  pause  (0'64  and  0"65  second)  than  that  of  the  other 
physiological  beats  (0*60  second).  The  a-c  interval  of  the  physiological 
beats  was  0"13  second.  A  week  later  extrasystoles  became  more  numer- 
ous, and  often  occurred  in  series  of  from  two  to  six  or  eight.  Some 
of  these  extrasystoles  were  of  ventricular  origin,  others  were  supra- 
ventricular (Fig.  68),  and  in  some  instances  a  ventricular  extrasystole 
was  followed  immediately  by  an  auricular  one.  At  the  same  time 
there  was  also  marked  sinus  irregularity,  and  this  together  with  the 
extrasystoles  rendered  the  arterial  pulse  markedly  irregular.  In  one 
record  the  intersystolic  periods,  estimated  from  a  brachial  tracing, 
were  0-86,  0-86,  0-52,  0-40,  0-40,  0-40,  0-45,  0-46,  0-50,  070,  0-70,  0-50, 
0-89,  0-90,  0-50,  0-40,  0-64,  0-44,  0-44,  0-50,  0-42,  0-92,  0-76,  .  .  .  0-45, 


CASE   VIII. 


61 


0-40,  1-30,  0-85,  0-74,  0-74,  0-50  second.     The  length  of  the  a-c  interval 
was  constantly  varying  from  0"15,  017,  or  0"1S  to  0"25  second. 

A  fortnight  later  the  extrasystolic  arrhytluiiia  became  replaced  by 
an  almost  absolutely  rhythmic  action  of  the  ventricles  at  a  rate  of 
113-120  per  minute,  this  being  associated  with  a  slight  degree  of 
pulsus  alternans  (Fig.  69).  The  auricles  were  probably  fluttering  at 
a  rate  of  226-240  per  minute.  This  condition  lasted  for  two  days. 
On  the  third  day,  when  the  patient  was  obviously  dying,  the  radial 


Fio.  Oi'. — The  ventricular  rate  is  114  per  minute,  and  there  is  slight  alternation  of  the  pulse. 
Apical  and  brachial  tracings.    Case  VII. 

pulse  could  hardly  be  felt,  the  rate  of  the  ventricles  rose  to  171-224 
per  minute  and  their  rhythm  became  extremely  irregular  (Fig.  70). 
An  intra-venous  injection  of  digitalin  failed  to  retard  the  ventricles, 
and  the  patient  died  the  same  evening.  Although  no  electrocardiograms 
or  satisfactory  jugular  tracings  could  be  obtained  during  the  last  three 
days  of  life,  the  sequence  of  extrasystolic  arrhythmia,  rhythmic  ven- 
tricular tachycardia,  and  gross   ventricular  irregularity,  suggests  that 


Fio.  70. — Pulsations  of  the  abdominal  aorta  at  a  rate  of  1ST  per  minute.     Case  VII.,  twelve  hours 
before  the  patient's  death. 

the  extrasystolic  arrhythmia  passed  into  auricular  flutter,  and  this  in 
turn  into  fibrillation. 

The  conditions  found  at  the  post-mortem  examination  have  been 
described  on  p.  32. 


Case  VIII. — Post-ixfluenzal  Tachycaedia  Persisting  for  some 
Months  ;  Improvement  under  Digitalin  ;  Patient  Well  Four 
Years  Later. 

The  patient  was  a  lawyer,  of  middle  age,  whose  professional  work 
had  been  arduous,  and  who  had  been  in  the  habit  of  taking  little  leisure 
or  recreation.     His  previous  health  had  been  uuiformly  excellent,  and 


62  ~  EECOEDS   OF   CASES 

he  never  had  occasion  to  consult  a  doctor  until  he  became  laid  up  with 
influenza  early  in  January  1905. 

When  I  saw  him  for  the  iirst  time  on  the  last  day  of  March  1905 
he  stated  that  ever  since  the  influenzal  attack  he  had  been  greatly 
troubled  with  nervousness,  insomnia,  palpitation,  and  perceptible 
irregularity  of  the  heart.  He  did  not  look  seriously  ill,  and  was 
neither  cyanotic  nor  dropsical.  His  heart  was  not  enlarged  and  no 
valvular  murmurs  were  audible,  but  the  first  sound  at  the  mitral  area 
was  reduplicated.  The  lungs  and  abdominal  viscera  were  healthy. 
The  patient  was  taking  strophanthus  and  strychnine,  yet  his  ventricular 
rate  was  usually  about  125-140  per  minute;  the  rhythm  was  some- 
times, but  not  constantly,  regular.  At  times  the  ventricular  rate  rose 
to  about  170  per  minute,  and  the  pulse  was  then  alternating. 

The  patient  was  extremely  nervous  about  himself,  slept  poorly  in 
spite  of  hypnotics,  and  was  liable  to  attacks  of  sweating  and  of  retching. 
His  condition  continued  unchanged  for  eighteen  days,  when  ^wo  grain 
of  digitalin  four  times  daily  was  substituted  for  the  strophanthus  and 
strychnine.  The  pulse-rate  was  then  134  per  minute,  and  the  radial 
tracing  showed  frequent  rhythmic  alternating  beats  in  groups  which 
were  separated  from  one  another  by  a  pulse  period  equal  to  two  of  the 
frequent  beats.  The  ventricles  were  probably  responding  successively 
to  ...  2,  2,  4,  2,  2,  2,  4,  2,  2,  2,  2,  .  .  .  auricular  beats. 

After  the  patient  had  taken  digitalin  for  three  weeks  his  condition 
was  greatly  improved.  His  appetite  was  good,  he  slept  soundly,  and 
he  was  able  to  be  out  for  a  drive  each  day.  His  pulse  was  then 
rhythmic  at  a  rate  of  100  per  minute.  Eour  years  later  the  patient 
was  reported  to  be  in  excellent  health  and  able  for  all  his  pro- 
fessional work. 

Case  IX. — Probable  Onset  of  Aupjcular  Flutter  at  a  Eate  of 
454  PER  Minute  during  Chloroform  An.^sthesia.^ 

Male,  aged  19,  under  the  care  of  Mr.  Cathcart  in  the  Eoyal 
Infirmary.  Eecords  were  taken  before  and  during  an  operation  for 
osteomyelitis  of  the  femur.  Twenty-five  minutes  before  the  anesthetic 
was  given  the  auricles  and  ventricles  were  beating  rhythmically  at  a 
rate  of  81  per  minute.  Seventeen  minutes  after  the  commencement  of 
administration  of  chloroform  they  were  beating  rhythmically  at  a  rate 
of  75  per  minute.     Thirteen  minutes  later  (1.33  p.m.)  the  pulse  was 

1  "Auricular  Flutter,"  Edin.  Med.  Journ.,  Ediu.,  1912  (N.  S.),  ix.,  485. 


CASE   X.  63 

markedly  liyperdicrotic  and  alternating,  and  its  rate  was  166.  At  1.34 
and  1.35  the  rates  were  194  and  176  respectively;  the  rhythm  was 
still  regular,  and  alternation  was  pronounced.  At  1.36  the  rate  of  the 
pulse  had  risen  to  227-230'7  pur  minute ;  it  was  still  rhytlnnic  and 
alternating.  The  jugulo- carotid  tracing  presented  a  continuous  series 
of  large  waves  at  a  rate  of  454  per  minute.  The  auricles  were  probably 
in  flutter.  The  rhythmic  tachycardia  persisted  at  about  the  same  rate 
for  three  minutes.  The  patient  then  became  cyanosed,  tlie  administra- 
tion of  the  anesthetic  was  stopped,  and  artificial  respiration  was  per- 
formed. At  1.40  the  pulse,  which  had  been  alternating  and  rhythmic, 
became  wholly  irregular.  The  pulse  periods,  estimated  from  the 
tracing,  were  0-32,  0-30,  0-52,  0-56,  0-35,  0-40,  0-38,  0-30,  0-40, 
0"44  second.  At  that  time  the  auricular  flutter  had  apparently  passed 
into  fibrillation.     Two  minutes  later,  however,  the  auricles  and  ventricles 


Fio.  Vl. — Rhythmic  tachycardia  at  a  rate  of  225  per  minute.    Case  IX. 

had  resumed  their  rhythmic  action  at  a  rate  of  125  per  minute,  and 
this  condition  lasted  until  the  record  ceased.  The  patient's  subsequent 
progress  was  uneventful. 

In  Case  II.,  with  undoubted  auricular  flutter,  the  arterial  pulse  was 
frequent,  rhythmic,  and  alternating,  and  was  associated  with  a  jugular 
pulse  of  ventricular  form.  The  same  phenomena  were  recorded  in  the 
following  case,  which  is  therefore  regarded  as  auricular  flutter. 

Case  X. — Arteeio-sclekosis  with  Heaet  Failure;   the  Auricles 

WERE   PROBABLY   FLUTTERING   AT   A   PtATE   OF    262   PER   MlNUTE.^ 

The  patient,  a  grocer,  aged  60  years,  was  seen  on  the  5th  September 
1912.  He  was  a  married  man,  of  careful  habits,  and  he  had  not  been 
intemperate.  He  had  been  a  very  active  man,  leading  a  busy  life,  until 
at  the  age  of  59  he  began  to  suffer  from  palpitation.  He  had  never 
experienced  any  cardiac  pain.     Dropsy  had  become  progressively  worse 

1  "Auricular  Flutter,"  Edin.  Med.  Journ.,  Edin.,  1912  (N.  S.),  ix.,  485. 


64  -  EECORDS   OF   CASES 

in  spite  of  rest  iu  bed,  digitalis,  and  diuretin.  When  I  saw  the  patient, 
one  year  after  his  illness  began,  he  was  confined  to  bed.  His  heart  was 
moderately  enlarged,  the  right  border  being  in  the  right  lateral  sternal 
line,  and  the  apex-beat  being  in  the  fifth  left  intercostal  space  half  an 
inch  outside  the  mammillary  line.  On  auscultation  a  high-pitched 
systolic  mitral  murmur  was  audible.  The  second  sound  was  loudly 
accentuated.  A  considerable  degree  of  pulsation,  which  was  of  ven- 
tricular form,  was  visible  in  the  jugular  veins  on  the  right  side  of  the 
neck  (Fig.  72).  The  walls  of  the  arteries  were  thick,  and  the  systolic 
pressure  was  275  mm.  Hg.  The  ventricles  were  beating  rhythmically 
at  a  rate  of  131  per  minute,  and  the  arterial  pulse  was  alternating 
(Fig.  72).  The  auricles  were  probably  fluttering  at  a  rate  of  262  per 
minute.  The  patient  died  about  one  month  after  the  record  in  Fig.  72 
was  obtained. 


Fig.  72. — Rhythmic  tachycardia  at  a  rate  of  131  per  minute,  with  a  ventricular  venous  pulse.    Case  X. 

Case  XL — Aueicular  Fluttee  at  a  Eate  of  285  per  Minute; 
Heaet  Failure;  Death. 

The  patient,  aged  65,  who  was  under  the  care  of  Dr.  Lovell  Gulland 
in  the  Royal  Infirmary,  had  a  persistent  and  rhythmic  tachycardia  at 
a  rate  of  about  140  per  minute  for  twelve  weeks  before  his  death.  No 
murmurs  were  audible.  Digitalis,  even  although  given  in  large  doses,, 
failed  to  retard  the  heart.  QLdema  and  bilateral  hydrothorax  developed, 
and  the  patient  gradually  sank,  and  died  eighteen  days  after  the  records 
in  Plate  XII.,  Figs.  63  and  64,  had  been  obtained.  The  post-mortem 
appearances  have  been  described  on  p.  33. 

Electrocardiograms  by  derivations  II.  and  III.  are  shown  in  Figs. 
63  and  64.  The  ventricles  are  beating  rhythmically,  in  response  to 
supra-ventricular  stimulation,  at  a  rate  of  142*8  per  minute.  The 
auricles  are  beating  rhythmically,  and  twice  as  fast  as  the  ventricles. 
One  auricular  deflexion  precedes  the  initial  ventricular  deflexion  by 
0'06-0'07  second ;  in  Fig.  63  the  second  auricular  deflexion  is  mingled 
with,  and  therefore  masked  by,  the  terminal  ventricular  deflexion,  but 
in  Fig.  64,  by  derivation  III.,  both  auricular  deflexions  are  visible. 


CASES   XIL,  XIII.  65 

Turning  from  the  cases  of  my  own  series,  it  is  found  that  forty-two 
other  cases  of  auricular  llutter,  making  a  total  of  fifty-three,  have  been 
recorded.  A  brief  summary  of  the  important  features  of  these  cases 
may  be  given. 

Case  XII. — Chronic  PEiucArxDiTis,  Heart  Failure,  and  Partial 
Heart-block;  Onset  of  Auricular  Flutter  Seven  Weeks 
before  Death. 

This  case  I  had  frequent  opportunities  of  observing  while  I  was 
attached  as  clinical  tutor  to  the  clinic  of  the  late  Dr.  George  A.  Gibson. 
He  recorded  the  case  in  1906.'^  The  patient,  who  was  a  dairyman  aged  44 
and  had  been  a  heavy  drinker,  had  been  breathless  for  two  years  before 
he  was  admitted  to  hospital  in  October  1904.  He  made  a  speedy  and 
satisfactory  recovery.  When  re-admitted  on  the  24th  January  1906,. 
he  was  languid,  somnolent,  breathless  and  jaundiced,  and  had  been 
suffering  from  palpitation.  The  right  and  left  borders  of  the  heart 
respectively  were  2^  and  4  inches  from  the  mid-sternal  line.  When 
the  auricles  were  in  flutter  the  ventricular  rate  was  usually  about 
40  per  minute,  the  rhythm  was  somewhat  irregular,  and  the  arterial 
pulse  was  weak.  The  systolic  pressure  was  93,  and  the  diastolic 
72  mm.  Hg. 

Eecords  taken  on  the  9th  February  (Fig.  2  of  Dr.  Gibson's  paper)- 
showed  that  the  auricles  were  beating  rhythmically  at  a  rate  of  200  per 
minute,  and  that  the  ventricles  responded  to  every  fourth,  or  every 
sixth,  auricular  beat.  A  portion  of  another  record  taken  on  the  same 
day  is  shown  in  Fig.  77.  Two  days  later  transient  paroxysmal  attacks 
of  flutter,  with  an  auricular  rate  of  nearly  350  per  minute,  alternated 
with  a  rhythm  that  was  physiological  in  every  respect  except  that  the 
rate  was  somewhat  frequent  (90  per  minute)  and  an  occasional  stimulus 
to  the  ventricles  was  b  oeked.  A  few  days  later  the  auricular  flutter, 
at  a  rate  of  about  350  per  minute,  became  apparently  continuous,  and 
nine  weeks  after  the  patient's  admission  to  hospital  he  died  somewhat 
suddenly.     The  condition  of  the  heart  has  been  described  on  p.  30. 

Case  XIII. — The  next  case  in  chronological  sequence  is  Morison's  - 
case  of  "jugular  embryocardia,"  observed  in  1903  and  recorded  in  1909. 

1  Gibson,  G.  A.,  "A  Discussion  on  some  Aspects  of  Heart-block,"  Brit.  Med. 
Journ.,  Lond.,  1906,  ii.,  1113. 

^  Morison,  A.,  "  Cardiac  Motion  as  Revealed  Ijy  the  Vivisection  of  Disease,"' 
Lancet,  Lond.,  1909,  i.,  77  ;  ibid.,  1909,  i.,  39. 

5 


66  EECOEDS   OF   CASES 

In  this  patient,  with  mitral  disease,  the  "  auricular  contractions  usually 
bore  to  ventricular  systole  the  ratio  of  208-228  :  108-114."  On  ausculta- 
tion over  the  jugular  area  sounds  were  persistently  heard,  which  in 
character  and  rate  very  strongly  resembled  those  of  the  foetal  heart. 
The  sounds  could  not  be  obliterated  by  pressure  of  the  stethoscope,  and 
were  assumed  to  be  due  to  right  auricular  and  venous  pulsation. 
During  the  patient's  residence  in  hospital  for  four  months  the  condition 
continued  uninterruptedly. 

Case  XIV. — In  the  case  described  by  Hertz  and  Goodhart^  in  1909, 
a  woman  aged  39  years,  who  was  affected  with  mitral  disease  and 
hemiplegia,  the  auricular  rate  was  almost  constantly  234  and  that  of 
the  ventricles  about  80  per  minute.  The  ventricular  beats  were  usually 
coupled.  Atropin  did  not  influence  the  auricular  beats,  whereas  the 
ventricular  rate  rose  from  78-84  to  150-170  per  minute,  two  and  a  half 
hours  after  an  injection,  and  fell  to  75  seventeen  hours  later.  The  rate 
of  the  auricles  was  likewise  uninfluenced  by  physical  exercise  or  by 
change  of  posture. 

Case  XV. — The  first  of  three  cases  recorded  by  Eihl.^  A  joiner, 
aged  55,  had  been  suffering  for  three  months  from  dyspnoea  on  exertion. 
Polygraph  tracings  and  electrocardiograms  demonstrated  an  auricular 
rate  of  285-300,  rising  on  one  occasion  to  315  per  minute.  The 
ventricular  rate  was  70-150  per  minute.  The  "auricular  tachysystole " 
was  not  retarded  by  digalen  or  by  vagus  compression,  but  both  induced 
ventricular  slowing.  This,  when  due  to  digalen,  could  be  abolished 
transiently  by  injection  of  atropin. 

Case  XVI. — Kibl's  second  case  was  a  waitress,  aged  32,  affected 
with  mitral  disease.  She  had  been  suffering  from  palpitation  and 
dyspnoea  for  one  year,  and  from  dropsy  for  one  month.  An  auricular 
rate  of  206-222  persisted  probably  for  about  eighteen  months,  and  the 
patient  became  markedly  dropsical  in  spite  of  diuretin,  digalen,  and 
other  remedies  being  administered.  The  ventricular  rate  was  usually 
52-72  per  minute,  but  there  were  occasional  paroxysms  in  which  the 
rate  rose  to  180-200  per  minute.  The  ventricular  rhythm  was  not 
uniformly  regular.     Vagus  compression  retarded  the  ventricles  only. 

1  Hertz,  A.  F.,  and  Goodhart,  G.  W.,  "  The  Speed-limit  of  tlie  Human  Heart," 
Quart.  Journ.  of  Med,  Oxford,  1908-9,  ii.,  213. 

2  Rihl,  J.,  "  Hocligradige  Vorhoftachysystolien  mit  Ueberleitungsstorungen  und 
electiver  Vaguswirkung,"  Zeitschr.  f.  exjMr.  Pathol  u.  Therap.,  Berlin,  1911,  ix.,  277. 


CASES   XVII.,  XVI II.,  XIX.  07 

Case  XA'II. — The  third  case  reported  by  Kiiil  was  a  labourer, 
aged  72,  who  was  seized  somewhat  suddenly  with  })alpitation,  cough, 
and  dropsy.  About  one  year  later  he  was  still  dropsical ;  his  heart  was 
much  enlarged.  His  auricular  rate  was  200-214  per  minute,  but  the 
ventricles  were  usually  beating  rhythmically  at  a  rate  of  100  per 
minute.  Vagus  compression  retarded  the  ventricles.  On  one  occasion 
there  was  a  paroxysm  in  which  the  ventricular  rate  rose  to  207  per 
minute.  When  this  attack  ended  the  pulse-rate  fell  suddenly  to  one- 
half  of  its  former  rate.  Infusion  of  digitalis,  caffein,  and  theobromin 
were  administered;  the  pulse  became  slower,  and  eventually  wholly 
irregular. 

Case  XYIII. — The  first  case  recorded  by  Mackenzie  ^  was  an  army 
officer,  born  in  1863,  who  had  no  rheumatic  or  specific  history.  In 
1902,  during  the  South  African  war,  he  first  became  conscious  of 
occasional  attacks  of  fluttering  in  the  chest.  They  did  not  cause  much 
distress  until  1905,  when  they  became  very  frequent  and  continued  for 
some  months.  In  1910  the  attacks  became  numerous  and  severe,  and 
the  patient  became  very  weak.  During  the  attacks,  which  were  pro- 
voked by  slight  exertion,  the  auricular  rate  probably  varied  only  from 
280-320 ;  the  ventricular  rate  was  130-150,  but  on  one  occasion  it 
rose  to  290-300  per  minute.  The  face  was  slightly  livid ;  the  sounds  of 
the  heart  resembled  the  tic-tac  of  the  foetal  heart.  Digitalis  produced 
auricular  fibrillation,  but  later  the  normal  rhythm  was  restored.  The 
patient  continued  to  take  half  a  drachm  of  digitalis  tincture  each  day, 
and  gradually  regained  strength.  Eventually  the  attacks  recurred  only 
at  rare  intervals,  and  did  not  last  for  more  than  a  few  minutes.  In 
1913  he  was  forced  to  lead  a  very  quiet  life,  as  exertion  induced  the 
rapid  heart  rate. 

Case  XIX.,  recorded  by  Mackenzie,"^  and  subsequently  by  TurubulP 
and  Lewis,^  was  a  man  aged  74  who  had  enjoyed  good  health  until,  on 
waking  one  morning,  he  felt  ill  and  was  found  to  have  a  very  rapid 

'  Mackenzie,  J.,  "Digitalis,"  Heart,  Lond.,  1910-11,  ii.  273,  Case  37  ;  Diseases  of 
the  Heart,  third  edition,  Lond.,  1913,  Appendix,  Case  55. 

2  Mackenzie,  .J.,  "Digitalis,"  Heart,  Lond.,  1910-11,  ii.,  273,  Case  38  ;  Diseases  of 
the  Heart,  third  edition,  Lond.,  1913,  Appendix,  Case  56. 

3  Tnrnbull,  H.  Hume,  "  Paroxysmal  Tachycardia  accompanied  by  the  Ventricular 
Form  of  Venous  Pulse,"  Heart,  Lond.,  1911-12,  iii.,  89, 

■*  Lewis,  T.,  "  Observations  upon  a  Curious  and  not  uncommon  Form  of  Extreme 
Acceleration  of  the  Auricle.     'Auricular  Flutter,'"  ibid.,  1912-13,  iv.,  171,  Case  15. 


68  EECOEDS   OF   CASES 

pulse.  About  three  months  later  he  was  cyanosed  and  dyspnoeic.  The 
heart  sounds  were  weak  but  clear.  The  ventricles  were  beating  rhyth- 
mically at  a  rate  of  150  per  minute.  The  jugular  pulsation  was  of  the 
ventricular  form,  "  though  after  an  occasional  pause  there  was  an 
auricular  wave  preceding  the  time  of  the  carotid."  Lewis  subsequently 
re-analysed  the  electrocardiograms  and  concluded  that  the  auricular  and 
ventricular  rates  respectively  were  280-300  and  140-150  per  minute. 

A  first  course  of  digitalis  in  considerable  doses  failed  to  arrest  the 
paroxysms  materially.  About  two  months  later  the  patient  took  33 
j^ativelle's  granules  in  the  course  of  eleven  days.  On  the  twelfth  day  the 
pulse  had  fallen  to  76,  being  at  times  regular,  at  others  irregular.  Five 
days  after  the  digitalis  was  discontinued  the  pulse  became  perfectly 
regular,  and  the  jugular  tracing  presented  a  well-marked  auricular  wave 
at  its  normal  instant.  It  was  not  until  three  days  later,  however,  that 
the  dyspnoea  and  delirium  vanished,  and  the  patient  really  felt  well.  The 
heart's  rate  was  then  72  per  minute,  and  except  for  an  occasional  extra- 
systole  the  rhythm  was  normal.  Thereafter  he  steadily  improved  and 
became  able  to  walk  a  distance  of  three  miles,  mostly  uphill,  without 
any  distress.  Three  years  later  he  was  still  in  good  health  and  had  no 
trouble  with  his  heart. 

Case  XX.,  recorded  by  Lewis  and  Schleiter,^  and  subsequently  by 
Lewis. ^  The  patient  was  a  cabinetmaker,  aged  28,  who  had  suffered 
from  paroxysmal  attacks  of  auricular  fibrillation  or  flutter.  They  were 
accompanied  by  palpitation,  dyspnoea,  fainting,  fatigue,  salivation, 
sweating,  sickness,  and  great  prostration.  One  attack  of  flutter  lasted 
for  twelve  hours.  On  another  occasion  an  attack  of  auricular  fibrillation 
lasting  for  three  and  a  half  days  became  transformed  into  flutter,  and 
the  latter  terminated  spontaneously,  Eecords  showed  an  auricular  rate 
of  280  with  a  ventricular  rate  of  140  per  minute. 

Case  XXI.  (Case  2  of  the  series  recorded  by  Lea^). — The  patient 
was  a  postman,  aged  57  years,  whose  previous  health  had  been  excellent. 
For  seven  months  he  had  been  suffering  from  dyspnoea,  and  subsequently 
he  suffered  from  transient  dropsy.  He  had  also  complained  of  pre- 
cordial pain  and  "  throbbing "    over  the   heart.      No   murmurs  were 

1  Lewis,  T.,  and  Sclileiter,  H.  G.,  "The  Relation  of  Regular  Tachycardias  of 
Auricular  Origin  to  Auricular  Fibrillation,"  Heart,  Lond.,  1911-12,  iii.,  173, 

2  Lewis,  T.,  ibid.,  1912-13,  iv.,  171,  Case  16. 

^  Lea,  C.  E.,  "Four  Cases  of  Auricular  Tachycardia,"  Pi'oc.  Royal  Soc. Med.,  Lond., 
1913,  vi,,  Med.  Sect,,  14, 


CASES   XXL,  XXIL  G9 

audible.  The  auricles  and  ventricles  were  beating  rliytlniiically  at 
rates  of  2G0  antl  130  per  minute  respectively. 

Under  the  inliuence  of  digitalis  the  auricular  frequency  was  not 
lessened,  but  the  ^'eutricular  rate  fell  to  one-third  of  the  auricular, 
and  occasionally  the  ventricular  rhythm  became  irregular  owing  to 
the  ratio  of  As  :  Vs,  varying  between  1  : 1,  2  : 1,  3  : 1,  4 : 1,  5  : 1,  and  6  : 1. 
Twelve  days  later  the  auricles  and  ventricles  were  beating  with  a 
physiological  rhythm  at  a  rate  of  65  per  minute,  but  when  the  patient 
moved  his  arms  up  and  down  for  a  little  time  the  auricles  relapsed  into 
tiutter.  After  the  patient  had  been  under  observation  for  nearly  five 
months  the  auricles  were  still  fluttering  and  the  ventricles  beating  at  a 
rate  of  130  per  minute. 

The  patient  was  then  leading  a  quiet  life,  taking  no  drugs  and 
keeping  in  fairly  good  health.  Dr.  Lea  in  a  personal  communication 
tells  me  that  the  patient  died  suddenly  in  June  1913,  about  nineteen 
months  after  the  commencement  of  his  illness. 

In  Case  4  of  Lea's  ^  series,  a  woman  aged  50,  suffering  from  lympho- 
cythffimia,  there  were  frequent  paroxysms  during  the  last  five  weeks  of 
life,  in  which  the  rate  of  the  rhythmically  beating  ventricles  changed 
abruptly  from  90  to  180  per  minute.  The  auricles  were  probably 
fluttering  at  a  rate  of  360  per  minute,  and  the  onset  of  a  paroxysm 
probably  denoted  a  change  of  the  auriculo-ventricular  ratio  from  4 : 1  to 
2:1.  At  the  post-mortem  examination  the  heart  was  apparently  fatty. 
In  a  personal  communication  Dr.  Lea  informs  me  he  has  seen  four  other 
cases  in  which  the  auricles  were  probably  fluttering. 

Case  XXIL — Lewis'^  has  recorded  eight  cases  of  auricular  flutter. 
His  first  case,  a  woman  aged  50  years,  had  suffered  from  acute  rheuma- 
tism at  the  age  of  23,  from  some  dyspnoea  for  eleven  years,  and  from 
notable  dyspnoea  and  palpitation  for  four  months.  She  also  complained 
of  precordial  pain.  She  was  cyanosed,  but  not  dropsical;  a  systolic 
murmur  was  audible  over  the  apex  of  the  heart.  The  attack  of  rapid 
heart  action  had  a  probable  duration  of  three  months.  Auricular  rates 
of  300,  314,  and  324  were  recorded  in  electrocardiograms.  The  ven- 
tricular rate  was  usually  one-half  of  the  auricular. 

After  the  patient  had  taken  18  drachms  of  digitalis  tincture  in 
eighteen  days,  the  ventricular  rate  fell  to  one-fourth  of  the  auricular. 

1  Lea,  C.  E.,  "  Four  Cases  of  Auricular  Tachycardia,"  Proc.  Royal  Soc.  Med.,  Lond., 
1913,  vi.,  Med.  Sect.,  14. 

2  Lewis,  T.,  "  Observations  upou  a  Curious  and  not  uncommon  Form  of  Extreme 
Acceleration  of  the  Auricle.     'Auricular  Flutter,'"  Heart,  Lond.,  1912-13,  iv.,  171. 


70  EECOEDS   OF   CASES 

Subsequently  auricular  fibrillation  ensued,  and  the  ventricular  rate  fell 
to  79  per  minute.  The  drug  was  then  discontinued.  A  week  later  the 
lieart  regained  its  physiological  rhythm,  and  the  patient's  symptoms 
were  considerably  relieved. 

Case  XXIII. — The  second  case  recorded  by  Lewis  ^  was  a  clergy- 
man, aged  65,  who  had  been  liable  to  paroxysmal  attacks  of  tachycardia 
for  thirty  years.  In  one  attack,  persisting  for  five  months,  the  auricular 
rate  was  266  to  289  per  minute.  The  ventricular  rate  was  usually  one- 
half,  but  sometimes  one-third  of  the  auricular  rate.  After  485  minims 
of  digitalis  tincture  had  been  administered  in  the  course  of  nine  days, 
the  auricles  were  alternately  fluttering  and  fibrillating ;  but  two  days 
after  the  drug  was  discontinued  the  auricular  fibrillation  was  probably 
continuous.  On  the  third  day  the  physiological  rhythm  was  regained, 
and  the  patient's  general  condition  improved  considerably.  A  few  weeks 
later,  however,  the  auricular  flutter  returned,  and  the  patient  died. 

Case  XXIV.,  the  third  case  of  Lewis's^  series,  was  a  clergyman, 
aged  53,  who  had  experienced  attacks  of  palpitation  and  rapid  heart 
action  for  thirty-eight  years.  The  attacks  had  been  more  frequent  and 
severe  since  he  suffered  from  diphtheria  at  the  age  of  41.  An  auricular 
rate  which  varied  between  264  and  324  was  persistent  during  the  seven 
weeks  while  the  patient  was  under  continuous  observation.  Meanwhile 
the  ventricles  responded  to  every  alternate  auricular  beat.  Neither 
digitalis  nor  strophanthus  arrested  the  flutter.  Under  the  former  drug, 
however,  the  ventricular  rate  was  retarded,  and  its  rhythm  became 
irregular.     Compression  of  the  left  vagus  retarded  the  ventricles  only. 

Case  XXV. — The  fourth  case  recorded  by  Lewis  ^  was  a  traveller, 
aged  62,  who  developed  continuous  tachycardia  during  an  attack  of 
"influenza."  About  two  months  later,  the  rate  of  the  auricles  and 
ventricles  respectively  was  270  and  135  per  minute.  The  patient 
became  cyanosed  and  breathless,  and  his  heart  was  enlarged.  Digi- 
talis and  strophanthus  slowed  the  ventricles,  but  had  no  influence  on  the 
fluttering  auricles.  Auricular  fibrillation  did  not  ensue.  Both  right 
and  left  vagus  compression  slowed  the  ventricles,  without  affecting  the 
auricles.  Six  months  after  the  flutter  was  first  recorded  the  auricles 
were  still  fluttering. 

1  Lewis,  T.,  "  Observations  upon  a  Curious  and  not  uncommon  Form  of  E.^ctreme 
Acceleration  of  the  Auricle.     'Auricular  Flutter,'"  Hearty  Lond.,  1912-13,  iv.,  171. 


CASES   XXVL,  XXVIL,  XXVIII.  71 

Case  XXVI. — The  fifth  case  in  Lewis's  ^  series  was  a  french 
polisher,  aged  60  years,  who  liad  been  suffering  for  three  months  from 
periodic  attacks  of  breathlessness.  He  was  cyanosed,  and  the  heart  and 
liver  were  enlarged.  The  auricular  and  ventricular  rates  were  300  and 
150  per  minute  respectively.  Compression  of  either  vagus  retarded  the 
ventricles  only.  Digitalis  changed  the  ratio  of  As :  Vs  from  2 : 1  into 
4  : 1,  and  thereafter  induced  auricular  fibrillation.  The  drug  was  discon- 
tinued ;  the  fibrillation  apparently  persisted  for  twenty-three  days,  and 
thereafter  the  physiological  rhythm  was  restored.  The  patient's  condi- 
tion had  now  become  greatly  improved;  his  colour  was  good,  his 
breathing  easy,  and  the  hepatic  enlargement  had  disappeared. 

Seven  weeks  later  the  auricular  flutter  recurred,  and  was  observed 
on  several  occasions  during  a  period  of  over  four  months.  The  flutter 
was  now  uninfluenced  by  digitalis,  but  the  cardiac  pain,  dyspnoea,  pal- 
pitation and  dropsy,  which  had  recurred,  w^ere  relieved.  Sixteen  days 
after  digitalis  was  discontinued,  and  nine  days  after  the  patient's 
discharge  from  hospital  his  auricles  were  fibrillating.  One  month 
later  the  physiological  rhythm  of  the  heart  was  found  to  have  been 
regained. 

Case  XXYII. — The  sixth  case  recorded  by  Lewis  ^  was  an  actor, 
aged  47,  who  had  suffered  for  many  years  from  sudden  attacks  of 
palpitation  under  the  influence  of  exercise  or  emotion,  and  who  was 
affected  with  chronic  articular  gout.  The  heart  was  of  normal  size,  but 
the  aortic  arch  was  somewhat  dilated.  The  auricular  rate  was  330,  the 
ventricular  rate  165  per  minute. 

Case  XXVIII.,  recorded  by  Mackenzie,-  and  apparently  the  seventh 
case  of  the  series  reported  by  Lewis.^  A  healthy  looking  man,  aged  53, 
had  been  conscious  of  intermittent  action  of  his  heart  since  the  age 
of  19,  but  of  late  years  the  "  heart  attacks  "  had  altered  somewhat  in 
character.  They  might  come  on  unexpectedly,  without  any  assignable 
cause,  and  might  last  for  an  hour  or  for  several  days.  The  ventricular 
rate  used  to  rise  suddenly  from  67  to  130-140  per  minute.  Electro- 
cardiograms showed  an  auricular  rate  of  228,  and  a  ventricular  jate  of 
114  per  minute.     The  area  of  cardiac  dulness  was  not  enlarged,  and  the 

1  Lewis,  T.,  "  Observations  upon  a  Curious  and  not  uncommon  Form  of  Extreme 
Acceleration  of  the  Auricle.     'Auricular  Flutter,'  "  Heart,  Lond.,  1912-13,  iv.,  171. 

2  Mackenzie,  J.,  Diseases  of  the  Heart,  third  edition,  Lond.,  1913,  Appendix, 
Case  .59. 


72  EECOEDS   OF   CASES 

sounds  were  normal.  Eest  in  bed  and  the  administration  of  digitalin 
relieved  the  patient  of  bis  symptoms ;  and  about  one  year  later  he  was 
reported  to  have  enjoyed  good  health,  though  there  had  been  occasional 
attacks  of  a  few  hours'  duration. 

Case  XXIX.,  the  last  case  of  Lewis's  ^  series,  was  a  clergyman,  aged 
52,  suffering  from  dyspnoea  and  weakness.  The  heart  was  enlarged,  but 
no  murmurs  were  audible.  The  auricles  were  beating  rhythmically  at  a 
rate  of  260  per  minute.  The  ratio  of  As :  Vs  was  as  a  rule  2 : 1,  but 
occasionally  3:1  or  4  : 1. 

Case  XXX. — The  case  recorded  by  Hume  ^  was  a  labourer,  aged  63, 
without  any  rheumatic  or  venereal  history,  who  for  three  or  four  months 
had  been  troubled  with  dyspnoea  and  giddiness.  His  heart  was  enlarged, 
and  there  was  auscultatory  evidence  of  mitral  incompetence.  The  sys- 
tolic blood-pressure  was  260  mm.  Hg.  The  ventricular  rate  was  about 
87,  with  a  ratio  of  As  :  Vs  : :  3  : 1.  A  week  later  varying  ratios  of  2:1, 
3:1,  and  4  : 1  alternated  with  a  more  persistent  3  : 1  ratio.  Under  digitalis 
the  auricular  rate  remained  at  260  per  minute,  but  a  continuous  auriculo- 
ventricular  ratio  of  4 : 1  became  established.  The  ventricular  retardation, 
however,  could  be  relieved  by  atropin.  Auricular  fibrillation  eventually 
supervened  and  became  persistent. 

Case  XXXI. — Goteling  Vinnis  ^  records  two  tracings  (Figs.  9  and  10 
of  his  paper)  showing  large  auricular  waves,  not  wholly  rhythmic,  at  a 
I'ate  of  350  per  minute,  from  a  case  of  paroxysmal  arrhythmia.  The 
illustration  s  leave  little  doubt  that  the  case  was  one  of  auricular  flutter 
in  which  the  ventricles  responded  irregularly. 

Case  XXXII. — In  the  first  of  the  two  cases  recorded  by  Hay^  the 
records  extended  over  a  period  of  about  seven  years.  The  patient,  aged 
46,  had  been  intemperate  and  had  suffered  from  smallpox  and  malaria. 
He  was  dyspnojic,  cyanosed,  and  dropsical.  Auricular  flutter  at  a  rate 
of  240  per  minute,  with  an  auriculo-ventricular  ratio  of  3 : 1  and  occa- 

^  Lewis,  T.,  "  Observations  upon  a  Curious  and  not  uncommon  Form  of  Extreme 
Acceleration  of  the  Auricle.     '  Auricular  Flutter,' "  Heart,  Lond.,  1912-13,  iv.,  171. 

2  Hume,  W.  E.,  "  A  Case  in  which  a  High  Speed  of  the  Auricles  did  not  produce 
Tachycardia,"  Quart  Jozirn.  of  Med.,  Oxford,  1912-13,  vi.,  235. 

3  Vinnis,  E.  W.  Goteling,  "  De  volkomen  onregelmatige  Hartswerking,"  Nederl. 
Tijdschr.  v.  Geneesk,  Amsterdam,  1913,  Ivii.,  501. 

*  Hay,  J.,  "  Two  Cases  of  Auricular  Flutter,"  Lancet,  Lond.,  1913,  ii.,  986. 


CASES   XXXIIL,  XXXIV.  73 

sional  irregularity  of  the  ventricles,  was  recorded.  Alternation  of  the 
pulse  was  pronounced  at  first,  but  subsequently  disappeared.  At  a  later 
stage  a  4 : 1  ratio  was  observed,  and  still  later,  under  the  influence  of 
squill,  auricular  fibrillation  supervened.  The  patient  left  hospital  greatly 
improved  and  began  regular  work.  Four  and  a  half  years  later  the 
normal  rhythm  of  the  heart  was  found  to  be  restored,  and  the  patient 
was  able  to  earn  a  living. 

Case  XXXIII. — The  second  case  recorded  by  Hay  ^  was  a  man 
aged  62,  whose  heart  was  much  enlarged  but  who  was  not  dropsical. 
Auricular  rates  of  261  and  300  per  minute  were  recorded,  with  ventri- 
cular rates  of  50-87  per  minute.  The  auriculo-ventricular  ratio  was 
usually  3:1,  but  this  was  occasionally  interrupted  by  ratios  of  6:1,  4:1. 
Digitalis  did  not  retard  the  auricles  or  induce  fibrillation,  but  it  lowered 
the  rate  of  the  ventricles  to  31  per  minute.  The  patient  continued  to 
take  10  minims  of  the  tincture  each  night,  this  dose  being  sufficient  to 
steady  his  ventricles.  About  five  months  later  the  rhythm  was  found 
to  be  perfectly  normal  except  for  numerous  auricular  extrasystoles. 

A  series  of  over  thirty  cases  has  been  examined  by  Mackenzie,^  who 
has  described  fully  the  clinical  features  of  auricular  flutter.  In  the 
appendix  to  his  monograph  Mackenzie  gives  a  detailed  account  of  fifteen 
cases  (Xos.  55-69)  in  which  the  diagnosis  was  confirmed  by  the  electro- 
cardiograph. Facts  regarding  some  of  these  cases  have  been  recorded 
elsewhere  either  by  Mackenzie  himself  or  by  other  writers  (see  Cases 
VI.,  XVIIL,  XIX.,  XXIV.,  XXV.,  XXVIIL,  XXIX.,  and  XXXIIL), 
but  the  series  includes  at  least  seven  new  cases. 

Case  XXXIV.^ — Male,  aged  61,  had  an  attack  of  influenza  and 
pneumonia,  and  the  heart  was  found  to  be  rapid  and  irregular.  Five 
months  later  he  complained  of  a  sense  of  constriction  in  the  precordial 
region.  His  pulse  was  144  and  its  rhythm  disorderly ;  the  legs  and  the 
bases  of  both  lungs  became  oedematous.  Under  the  influence  of  digitalis 
the  patient's  condition  improved,  though  he  had  occasional  attacks  of 
tachycardia,  and  in  one  attack  he  felt  very  faint  and  almost  lost  con- 
sciousness. On  one  occasion  his  auricles  were  sometimes  in  flutter, 
sometimes  in  fibrillation,  and  then  for  a  short  time  the  rhythm  would 

1  Hay,  J.,  "Two  Cases  of  Auricular  Flutter,"  Lancet,  Loud.,  1913,  ii.,  986. 

2  Mackeuzie,  J.,  Diseases  of  the  Heart,  third  editiou,  Lond.,  1913,  237-250,  428-442. 

3  Mackenzie,  J.,  ibid.,  Appeudix,  Case  61. 


74  EECOEDS   OF   CASES 

be  perfectly  normal.     When  the  auricles  were  in  flutter  their  rate  was 
308,  while  the  ventricular  rate  was  154  per  minute. 

Case  XXXV.  (Case  64  of  Mackenzie's  series).^— In  this  case  auri- 
cular flutter  was  the  result  of  an  acute  infection.  The  patient,  a  man 
aged  47,  had  been  in  good  health  until  one  evening  he  became  feverish 
and  coughed  up  some  blood-stained  sputum.  On  the  next  day  he  was 
rather  breathless  and  dusky.  Three  days  later  there  was  an  attack  of 
great  breathlessness,  and  the  pulse  became  rapid,  irregular,  and  at  times 
scarcely  perceptible.  Above  each  clavicle  the  jugular  bulb  was  seen  and 
felt  beating  forcibly.  Crepitations  were  audible  at  the  bases  of  the 
lungs.  About  six  weeks  later  he  gradually  became  worse ;  Cheyne- 
Stokes  respiration  developed;  the  urine  became  scanty;  the  legs  and 
abdomen  became  dropsical;  and  the  patient  gradually  sank,  and  died 
four  months  after  the  onset  of  the  illness. 

In  this  case  the  recorded  auricular  rate  was  240  per  minute. 

Case  XXXVI.  (Case  65  of  Mackenzie's  series).- — Female,  aged  39, 
affected  with  syphilitic'  aortitis  and  myocarditis.  The  patient  was 
cyanosed,  breathless,  and  dropsical.  Systolic  and  diastolic  aortic  mur- 
murs were  audible.  After  the  onset  of  auricular  flutter  the  general 
symptoms  became  worse ;  no  change  w^as  found  in  the  area  of  cardiac 
dulness  or  the  characters  of  the  murmurs,  but  the  pulse  became  irregular. 
The  patient  died  about  six  months  after  the  initial  symptoms  of  heart 
failure  had  appeared  and  nineteen  days  after  the  onset  of  flutter. 

Case  XXXA^IL,  recorded  by  Mackenzie.^ — Male,  aged  63,  who  had 
probably  suffered  from  syphilis,  and  who  had  been  suffering  for  a  few 
months  from  cough  and  attacks  of  great  breathlessness.  Electrocardio- 
grams revealed  damage  to  the  right  branch  of  the  atrio-ventricular 
bundle.  After  he  had  been  ailing  for  about  three  and  a  half  years  he 
was  taken  seriously  ill  with  great  weakness  and  breathlessness.  He  lay, 
propped  up  in  bed,  in  a  slight  stupor  and  with  marked  Cheyne-Stokes 
respiration.  The  pulse  was  very  rapid,  and  varied  in  rhythm.  The 
characters  of  the  jugular  pulsations  indicated  auricular  flutter.  He 
gradually  sank,  and  died  a  month  later. 

1  Mackenzie,  .J.,  Diseases  of  the  Heart,  third  edition,  Lond.,  1913,  Appendix, 
Case  64. 

2  Op.  cit.,  Appendix,  Case  65. 
^  023.  cit.,  Appendix,  Case  66. 


CASES   XXXVlll.,  XXXIX.,  XL.  75 

Case  XXXVIII.,  recorded  by  ]\Iackenzie.^ — Male,  born  in  1833,  had 
enjoyed  good  health  until  1901,  when  he  began  to  have  attacks  of  loss 
of  consciousness.  As  a  rule,  these  attacks  came  on  suddenly ;  he  would 
fall  and  immediately  recover,  but  would  feel  dazed  and  weak.  Once  he 
lay  unconscious  for  several  hours,  with  a  pulse  so  small  that  the  doctor 
in  attendance  thought  he  was  dead  on  several  occasions.  About  six 
years  later  a  severe  attack  of  flutter,  with  a  pulse-rate  of  just  over  200 
per  minute,  occurred.  He  became  very  restless,  and  his  mind  wandered. 
Xo  remedies  were  efficacious.  During  the  succeeding  mouth  the  pulse- 
rate  usually  varied  in  rate  from  7-i  to  180 — being  sometimes  regular,  at 
other  times  irregular.  Slight  excitemoit  or  exertion  would  often  induce 
an  attack  of  very  rapid  heart  action,  and  the  patient  gradually  became 
weaker  and  died. 

Case  XXXIX.,  recorded  by  Mackenzie.- — Paroxysmal  tachycardia, 
probably  due  to  auricular  flutter.  Male,  aged  27,  had  suffered  from 
rheumatic  fever  on  two  occasions.  The  paroxysmal  attacks  used  to 
begin  suddenly.  At  first  they  were  infrequent  and  lasted  for  only 
a  few  minutes,  but  subsequently  they  occurred  every  few  weeks  and 
usually  lasted  from  half  an  hour  to  six  hours.  If  he  took  ipecacuanha 
wine  the  attacks  usually  ceased  after  he  was  sick  and  vomited.  Dur- 
ing the  course  of  a  third  attack  of  rheumatic  fever,  a  paroxysmal  attack 
started  and  persisted  for  five  days.  This  attack  promptly  ceased,  and 
the  patient  experienced  great  relief  after  vomiting  had  been  induced 
by  ipecacuanha.  Subsequently  he  said  he  could  stop  an  attack  by 
swallowing  and  belching  air.  This  procedure  was  found  to  induce 
a  slight  and  transient  degree  of  heart-block.  The  patient  gradually 
improved,  and  for  the  last  two  years  he  has  been  able  to  follow  his 
profession,  though  he  is  occasionally  liable  to  be  crippled  by  a  short 
attack. 

Case  XL.,  recorded  by  Mackenzie.^ — Female,  aged  16,  had  suffered 
from  rheumatic  fever,  and  for  some  years  she  had  complained  of  breath- 
lessness  and  palpitation  on  exertion.  The  records  sometimes  showed 
the  characteristic  features  of  auricular  fibrillation ;  at  other  times 
there  was  a  rapid  regular  rhythm  suggestive  of  auricular  flutter. 

1  Mackenzie,  J.,  Diseases   of  the  Heart,  third   edition,  Lond.,   1913,  Ajjpendix 
Case  67. 

-  Op.  cit.,  Appendix,  Case  68. 
^  Op.  cit,  Appendix,  Case  69. 


76  EECOEDS   OF   CASES 

Case  XLI.,  recorded  by  Fulton.^  —  The  patient  was  a  jeweller, 
aged  48,  suffering  from  progressive  chronic  nephritis.  For  a  year 
before  admission  to  hospital  he  had  been  breathless  on  exertion,  and 
for  five  weeks  he  had  been  dropsical.  After  he  had  been  in  hospital 
for  three  months,  he  suddenly  developed  an  irregular  action  of  the 
heart  which  persisted  for  a  month.  The  return  to  the  normal  rhythm 
was  sudden.  There  were  no  special  symptoms  during  the  attack, 
except  that  the  cedema  was  more  marked,  and  towards  the  end  of  the 
attack  Cheyne-Stokes  breathing  developed.  Digitalis  was  administered 
during  the  greater  part  of  the  attack,  and  meanwhile  the  auricles  were 
probably  fluttering  at  a  rate  of  286  to  308  per  minute.  At  first  the 
ventricles  responded  to  each  alternate  auricular  beat.  Subsequently 
the  ventricular  responses  were  irregular,  but  there  was  definite  and 
uniform  grouping  of  the  ventricular  beats,  similar  to  those  in  Fig.  104. 

Case  XLIL,  recorded  by  Fulton.^ — A  man,  aged  54,  with  gradually 
increasing  dyspnoea  and  oedema,  came  under  observation  with  chronic 
nephritis  and  an  enlarged  heart.  His  pulse,  at  a  rate  of  135  to  138 
and  with  marked  alternation,  was  not  influenced  by  posture  or  exercise. 
In  the  venous  tracing  the  rate  of  tlie  auricular  waves  was  272  per 
minute.  Eest  in  bed  induced  some  improvement  in  the  patient's 
general  condition,  but  the  pulse-rate  was  not  retarded  until  digipur- 
atum  had  been  given  for  eight  days.  The  pulse  then  became  slower 
and  irregular  in  consequence  of  impaired  and  irregular  conduction 
of  stimuli  to  the  ventricles.  About  one  month  later,  the  patient  was 
again  suffering  from  oedema  and  paroxysmal  attacks  of  dyspnoea,  and 
a  fortnight  later  the  auricles  were  in  fibrillation. 

Case  XLIIL,  recorded  by  Hume.^ — A  girl,  aged  7  years,  was 
admitted  to  hospital  on  the  fourth  day  after  the  onset  of  diphtheria. 
On  the  ninth  day  of  illness  auricular  extrasystoles  were  recorded.  On 
the  tenth  and  eleventh  days,  when  there  were  evident  signs  of  collapse, 
the  heart  was  beating  with  a  nodal  rhythm.  On  the  twelfth  day  the 
extremities  were  cold,  the  child  was  apathetic  and  pallid,  the  pulse-rate 
varied  from  90  to  102,  and  the  auricles  were  probably  in  flutter.  The 
child  died  three   days  later.      At  the  post-mortem  examination  the 

1  Fulton,  F.  T.,  "  '  Auricular  Flutter,'  with  a  Report  of  Two  Cases,"  Archives  of 
Intern.  Med.,  Chicago,  1913,  xii.,  475. 

2  Hume,  W.  E.,  "  A  Polygraphic  Study  of  Four  Cases  of  Diphtheria,  with  a 
Pathological  Examination  of  Three  Cases,"  Heart,  Loud.,  1913-14,  v.,  25. 


CASES   XLIV.  TO   XLVII.  77 

lungs  presented  patclies  of  bronclio-pnomnonia  and  of  collapse;  the 
kidneys  presented  acute  nepluitis.  The  heart-muscle  was  pale  and 
friable ;  the  valves  were  healthy.  Both  the  auricular  and  ventricular 
musculature  showed  fatty  degeneration,  and  in  the  ventricles  there  was 
also  a  gross  degree  of  interstitial  myocarditis.  The  atrio-ventricular 
node  and  bundle  appeared  to  be  perfectly  healthy. 

Case  XLIV.,  recorded  by  Hume,^  was  a  boy,  aged  5  years,  who 
was  suffering  from  diphtheria.  A  nodal  rhythm  was  recorded  on  the 
eighth  day  of  illness.  Two  days  later,  while  the  nodal  rhythm  per- 
sisted, signs  of  collapse  ensued.  Auricular  liutter,  at  a  rate  of  about 
500  per  minute,  and  with  a  ventricular  rate  of  96  to  132  per  minute, 
probably  supervened  on  the  eleventh  day,  two  days  before  the  child 
died.  The  musculature  of  the  auricles  and  ventricles  presented  fatty 
degeneration;  the  sinus  node  was  inflamed;  the  atrio-ventricular  node 
was  slightly  congested,  but  the  bundle  and  its  branches  were  healthy 
(see  also  p.  33). 

Cases  XLA".  and  XLVI.^ — Fahrenkamp  examined  a  series  of  cases 
of  "  arhythmia  perpetua,"  and  in  tw^o  instances  (Xos.  30  and  33  of  his 
series)  there  was  a  rhythmic  auricular  tachysystole.  The  first  case  was 
a  man,  aged  50,  affected  with  mitral  stenosis  and  incompetence  in  whom 
the  auricular  rate  was  240  to  350  (usually  300),  and  the  ventricular 
rate  58-82  per  minute.  The  second  case  was  a  man,  aged  47,  suffer- 
ing from  myocarditis,  mitral  stenosis,  and  mitral  incompetence.  The 
auricular  beats  were  rhythmic  at  a  rate  of  190  to  240  per  minute, 
whereas  the  ventricles  were  beating  irregularly  at  a  rate  of  only  50-60 
per  minute.  Slight  exertion  induced  a  paroxysm  in  which  the  ventricular 
rate  attained  the  same  frequency  as  that  of  the  auricles. 

Fahrenkamp  tabulates  thirty-six  other  cases  in  which  ventricular 
irregularity  was  associated  with  "  arhythmic  auricular  tachysystole " 
at  a  rate  of  about  300-400  per  minute.  In  these  cases  the  auricular 
deflexions  were  irregular  in  rhythm,  form,  and  amplitude,  and  may  be 
regarded  as  indicating  coarse  fibrillation  rather  than  auricular  flutter. 

Case  XLYII.^ — A  customs  officer,  aged  52,  who  had  been  a  temper- 

1  Hume,  W.  E.,  "A  Polygrapbic  Study  of  Four  Cases  of  Diplitheria,  \\itli  a 
Patliological  Examination  of  Three  Cases,"  Heart,  Lond.,  1913-14,  v.,  25. 

-  Falirenkamp,  K.,  "  Ueber  das  Elektrokardiogramm  der  Arhythmia  perpetua," 
Deutsch.  Arch.  f.  Uin.  Med.,  Leipz.,  1913,  cxii.,  302. 

3  Mathewson,  G.  D.,  "  A  Case  of  Auricuhir  Flutter,'"  Edin.  Med.  Journ.,  Edin., 
1913  (X.  S.),  xi.,  500. 


78  EECOEDS   OF   CASES 

ate  man  and  had  never  been  ill  except  for  one  attack  of  acute  rheuma- 
tism at  the  age  of  26,  had  been  complaining  for  eight  months  of  pain 
in  the  region  of  the  stomach,  and  for  two  months  of  dyspnoea.  On 
rising  in  the  morning  he  had  often  suffered  from  palpitation  and 
giddiness.  He  had  remained  at  work,  however,  until  he  was  admitted 
to  the  Edinburgh  Eoyal  Infirmary. 

His  heart  was  dilated,  but  no  murmurs  were  audible ;  there  was 
no  cedema  of  the  feet  or  lungs,  and  no  albuminuria.  The  auricles  were 
fluttering  at  a  rate  of  298  to  312  per  minute.  The  ventricular  rate 
(156  to  164)  was  at  first  one-half  of  the  auricular  rate,  but  under 
treatment  with  digitalis  the  ventricular  responses  began  to  vary  from 
2:1  to  3:1,  and  thereafter  a  continuous  3 : 1  rhythm  was  established. 
On  the  ninth  day  of  treatment,  the  auricles  passed  into  fibrillation, 
with  an  irregular  pulse  at  a  rate  of  60-80  per  minute.  This  persisted 
for  four  weeks,  and  during  the  whole  of  this  period,  although  no 
digitalis  was  being  given,  the  patient  felt  well. 

At  the  end  of  one  month  the  auricular  flutter,  at  a  rate  of  298- 
312  per  minute,  reappeared  suddenly  with  symptoms  of  giddiness  and 
faintness,  and  with  a  ventricular  rate  one-half  that  of  the  auricles. 
Digitalis  had  the  same  effect  as  before  in  slowing  the  ventricles,  and 
ultimately  in  producing  auricular  fibrillation.  This  persisted  until 
the  patient  left  hospital,  his  general  condition  being  then  greatly 
improved. 

Cowan  ^  records  three  cases,  and  refers  to  four  others  in  which  the 
polygraphic  records  seemed  clearly  to  prove  flutter. 

Case  XLVIII.  (Cowan's  first  case). — A  shipyard  labourer,  aged  51, 
had  been  suffering  for  one  year  from  paroxysms  of  palpitation,  giddiness 
and  shortness  of  breath,  and  from  a  gnawing  pain  in  the  epigastrium  for 
three  weeks.  He  became  very  weak  and  ill.  There  was  no  oedema, 
but  the  liver  was  large  and  somewhat  tender,  and  the  urine  contained 
albumin.  The  area  of  cardiac  dulness  measured  5|  inches  transversely ; 
the  sounds  were  muffled  and  indistinct,  but  pure.  At  the  outset  the 
ventricular  action,  at  a  rate  of  136  to  150,  was  extremely  irregular,  series 
of  5  to  20  beats  of  uniform  rhythm  and  force  being  separated  from  one 
another  by  pauses  of  longer  duration,  or  by  a  number  of  beats  at  a  less 
frequent  rate.  The  pulse-rate  fell  suddenly  and  the  rhythm  became 
perfectly  regular.  The  patient  was  conscious  of  the  improvement  and 
of  the  cessation  of  the  flutter.     His  subsequent  progress  was  good ;  the 

1  Cowan,  J.,  Diseases  of  the  Heart,  Lond.,  1914,  cliap.  xvi. 


CASES   XLIX.,  L.,  LI.  79 

area  of  cardiac  dulness  rapidly  diminished  to  4]  inches,  and  tlie  hepatic 
engorgement  and  pain  passed  away. 

Case  XLIX. — The  second  case  recorded  by  Cowan  ^  was  a  wire- 
drawer,  aged  61,  who  had  been  a  healthy  man  save  for  a  brief  attack 
of  dropsy  three  years  previously.  For  about  four  months  he  had  been 
complaining  of  nausea,  giddiness,  cough,  pain  in  the  chest,  and  paroxysms 
of  nocturnal  dyspnoea.  On  admission  to  hospital  he  was  dropsical ; 
there  was  difluse  bronchitis,  the  liver  was  enlarged,  double  aortic 
murmurs  were  audible,  and  the  Wassermann  test  was  positive.  About 
six  weeks  later  his  condition  became  worse.  His  ventricular  action  at  a 
rate  of  140  to  178  per  minute  was  perfectly  rhythmic,  and  the  diastolic 
murmur  disappeared.  The  ventricular  rate,  after  remaining  very 
frequent  for  eleven  days,  fell  suddenly  to  92,  and  afterwards  to  76. 
The  rhythm  was  then  notably  irregular,  and  the  auricles  were  in  fibril- 
lation. The  patient  had  been  taking  digitalis  meanwhile.  On  the 
following  day  the  frequent  cardiac  action  (140  to  174  per  minute) 
recurred  and  continued  for  eighteen  hours,  when  the  rate  fell  suddenly 
to  88.  The  rhythm  from  this  time  onwards  remained  wholly  regular, 
except  for  an  occasional  extrasystole. 

Case  L. — The  third  case  of  Cowan's^  series  was  a  lad,  aged  17, 
who  complained  of  attacks  of  palpitation,  which  he  dated  from  a  fright 
that  he  had  received  at  the  age  of  twelve.  For  two  months  the  attacks 
had  been  more  frequent;  he  had  become  breathless  on  exertion,  and 
easily  tired.  The  pulse-rate  varied  from  60  to  214.  The  paroxysms, 
which  began  and  ended  abruptly,  might  pass  off  in  a  few  minutes  or 
might  last  for  twenty-four  hours.  "When  the  paroxysms  ceased  the 
enlargement  of  the  right  heart  and  of  the  liver  speedily  disappeared. 
The  pulse-rate  was  always  increased  by  examination,  and  lessened 
during  sleep.  Digitalis,  opium,  belladonna,  and  compression  of  the 
vagus  seemed  to  have  little  influence  on  the  rate  of  the  heart. 

Case  LI.  (recorded  by  Hoffmann).- — A  somewhat  delicate  boy 
suffered  from  acute  gastro-enteritis  at  the  age  of  ten,  and  thereafter 
he  began  to  complain  of  cardiac  symptoms.  He  remained  in  fairly  good 
health,  however,  until,  at  the  age  of  fourteen,  his  heart's  action  became 

1  Cowan,  J.,  Diseases  of  the  Heart,  Lond.,  1914,  205,  207. 

-  Hotfniaim,  A.,  Die  Elektrograpliie  ah  Untersucliumjsmethode  (Us  Her>.ens  und  Hire 
Ergebnisse,  Wiesbaden,  1914,  188-193. 


80  KECOEDS   OF   CASES 

strikingly  irregular  after  a  slight  follicular  tonsillitis.  The  heart  was 
small,  the  sounds  were  pure,  the  pulse  soft  and  wholly  irregular  at  a 
rate  of  about  120  per  minute.  The  auricular  rate  was  about  280  per 
minute,  and  the  conduction  of  stimuli  to  the  ventricles  was  sometimes 
notably  depressed.  The  patient  was  under  observation  for  three  months, 
and  during  the  whole  of  this  period  the  flutter  persisted. 

Case  LII.^ — A  man,  aged  66,  had  an  attack  of  paroxysmal  tachy- 
cardia thirty-two  years  previously.  The  attack  was  brought  on  by 
severe  strain,  and  lasted  for  several  hours.  Thereafter  he  had  occasional 
attacks,  especially  after  drinking  cold  water  or  eating  indigestible  food. 
The  attacks  began  and  ended  suddenly,  and  usually  lasted  for  several 
hours.  During  the  attacks  the  pulse-rate  often  rose  to  140-160,  and 
occasionally  to  180  per  minute.  Even  during  the  attacks  he  had  no 
dyspnoea,  but  of  late  he  had  complained  of  sub-sternal  pain.  The  heart 
was  not  enlarged ;  the  aortic  curve  was  prominent ;  the  sounds  were  pure. 
The  auricles  were  beating  at  a  rate  of  300  per  minute,  with  an  auriculo- 
ventricular  ratio  of  2  : 1  or  3  : 1.  Compression  of  the  left  vagus  produced 
transient  slowing  of  the  ventricles  only. 

Case  LIII.^ — A  woman,  aged  65,  had  been  subject  to  slight  palpita- 
tion since  her  youth,  but  the  attacks  had  been  worse  since  the  age  of 
sixty.  The  heart  was  slightly  enlarged  to  the  left,  the  sounds  were 
pure,  but  the  second  sound  at  the  aortic  area  was  somewhat  accentuated. 
The  pulse-rate  was  164-176,  the  rhythm  was  regular,  and  the  auricles 
were  beating  at  twice  the  rate  of  the  ventricles.  Compression  of  the 
vagus  led  to  slowing  of  the  ventricles,  and  the  true  nature  of  the  auricular 
action  was  thereby  revealed.  Subsequently  the  patient  became  dropsical, 
and  she  died  suddenly. 

Digitalis  was  administered  to  the  three  cases  recorded  by  Hoffmann, 
but  the  drug  did  not  influence  the  ventricles,  and  auricular  fibrillation 
did  not  supervene. 

1  Hoffmann,  A.,  Die  Eleldrographie  als  UntersucMmgsmethode  des  Herzens  und  Hire 
Ergehmsse,  Wiesbaden,  1914,  193-202. 


CHAPTER  V 
CLINICAL  FEATURES 

Even  in  an  apparently  healthy  heart  the  onset  of  auricular  iiutter,  with 
pronounced  ventricular  acceleration,  greatly  impairs  the  efficiency  of  the 
organ,  and,  as  a  rule,  causes  distressing,  or  even  urgent,  symptoms.  In 
other  instances  the  myocardium  is  known  to  be  diseased,  and  grave 
indications  of  heart  failure  have  been  recognised  prior  to  the  onset  of 
auricular  flutter,  yet  when  this  disorder  does  ensue  all  the  patient's 
symptoms  become  aggravated. 

The  symptoms  specially  associated  with  auricular  flutter  are  not 
direct  manifestations  of  the  extreme  acceleration  of  the  auricles,  but 
are  due  to  ventricular  acceleration  and  to  secondary  alterations  in  the 
arterial  and  venous  pressures.  In  a  normal  heart  beating  at  a  rate  of 
75  per  minute  the  duration  of  ventricular  systole  is  about  0'30  second, 
and  that  of  ventricular  diastole  about  0*5  second.  When  the  auricles 
are  in  flutter  the  rate  of  their  contraction  is  usually  about  250-300 
per  minute,  whereas  the  ventricular  rate  is  usually  one-half  of  the 
auricular  rate.  In  auricular  flutter,  as  in  other  forms  of  tachycardia, 
the  ventricular  acceleration  occurs  mainly  at  the  expense  of  diastole, 
although  the  systolic  phase  may  also  be  curtailed  somewhat.  For 
example,  in  Case  II.,  with  auricular  and  ventricular  rates  of  283  and 
141'5  per  minute  respectively,  ventricular  systole  lasted  about  0'245 
second,  whereas  ventricular  diastole  lasted  only  0*175  second.  In 
Case  III.  the  duration  of  ventricular  diastole  was  reduced  to  about 
0"14  second. 

The  curtailment  of  ventricular  diastole  to  one-third,  or  less,  of  its 
normal  duration  does  not  necessarily  imply  imperfect  filling  of  the 
ventricles,  for  we  know  that  in  health  filling  is  almost  maximal  at  an 
early  period  of  diastole.  The  curtailment  of  diastole,  however,  entails 
a  period  of  rest  shorter  than  normal,  and  the  ventricles  are  again 
stimulated  to  contract  at  a  time  when  their  contractility  is  yet  only 
partially  restored.  The  ventricular  beats  are  therefore  enfeebled, 
the  arterial  pressure  must  necessarily  fall,  and  the  circulation  of 
blood  become  impaired  in  the  systemic  and   pulmonary  circulations. 

81  Q 


82  CLmiCAL   FEATUEES 

Moreover,  from  the  cyanosis,  cedema,  dropsy,  and  other  clinical  manifesta- 
tions, we  may  conclude  that  there  is  at  the  same  time  a  rise  of  venous 
pressure. 

In  considering  the  clinical  features  of  auricular  flutter  it  is  con- 
venient to  recognise  four  groups  of  cases — (1)  Auricular  flutter  in  an 
apparently  healthy  heart ;  (2)  auricular  flutter  supervening  during  the 
course  of  chronic  cardiac  disease ;  (3)  auricular  flutter  in  association 
with  partial  heart-block  ;  and  (4)  auricular  flutter  with  complete  heart- 
block.  Flutter  comes  on  in  the  form  of  paroxysmal  attacks  which  may 
subside  in  the  course  of  a  few  minutes,  or  may  persist  for  days,  months, 
or  even  years. 

I.  AuEicuLAR  Flutter  in  an  Apparently  Healthy  Heart 

In  an  individual  who  had  previously  enjoyed  good  health,  a  paroxysmal 
attack  of  flutter  may  be  excited  suddenly,  and  without  any  warning,  under 
the  influence  of  emotion  or  physical  exertion,  or  the  attack  may  appar- 
ently start  during  sleep,  the  patient  awaking  to  find  himself  ill  and  his 
pulse  greatly  accelerated.  In  some  instances  it  ma.y  be  possible  to  refer 
the  onset  of  the  attack  to  some  acute  infective  disease  or  toxaemia,  such 
as  influenza  or  gastro-intestinal  catarrh. 

Premonitory  symptoons,  due  mainly  to  extrasystoles,  may  have 
occurred  now  and  again  for  many  months  or  years.  There  may  have 
been  vague  and  momentary  sensations  of  discomfort  in  the  precordial 
region,  such  as  that  of  "  a  flapping  in  the  chest "  or  of  "  the  heart  stand- 
ing still,"  indicating  an  occasional  extrasystole.  Again,  the  occurrence 
of  multiple  extrasystoles  may  have  given  rise  to  the  alarming  symptom 
of  "  tremor  cordis  "  so  well  described  by  Balfour  ^  and  Gibson.^  In  this 
condition  the  patient  complains  of  "  fluttering  in  the  chest,"  of  "  flutter- 
ing of  the  heart,"  or,  as  Gibson  says,  "  the  individual  affected  feels  as  if 
he  had  a  timid  bird  fluttering  within  the  bosom."  The  rapid,  feeble,  and 
irregular  beats  of  the  ventricles  in  "  tremor  cordis  "  are  recognisable  by 
the  hand  laid  on  the  precordia,  as  well  as  by  the  ear.  The  attack  may 
last  for  a  few  seconds,  and  usually  ends  abruptly  with  a  pause  and  then 
an  unduly  forcible  beat. 

The  symptoms  of  auricular  jiutter  are  essentially  due  to  the  great 
acceleration  of  the  ventricles  under   the   influence   of   the   fluttering 

1  Balfour,  G.  W.,  Clinical  Lectures  on  Diseases  of  the  Heart  and  Aorta,  Lond., 
1898,  282. 

2  Gibson,  G.  A.,  The  Nervous  Affections  of  the  Heart,  Edin.  and  Lond.,  1904, 
92,  93. 


FLUTTElt    IX   AlTAltEXTLY   HEALTliV   HEAKTS        83 

auricles.  In  most  cases  the  initial  symptom  of  each  paroxysm  is 
palpitation,  which  is  often  very  distressing.  This  symptom  usually 
persists  while  the  ventricular  rate  remains  accelerated,  and  if  the  attack 
be  a  prolonged  one  the  patient  often  complains  of  dyspnoea,  precordial 
pain,  weakness,  and  prostration.  In  some  instances  vertigo  ensues  as 
a  result  of  the  weak  and  extremely  rapid  ventricular  action,  and  there 
may  be  occasional  syncopal  attacks.  These  are  most  apt  to  ensue  when 
the  ventricles  respond  to  each  auricular  beat  and  when  tlie  ventricular 
rate  therefore  rises  to  about  200  to  300  per  minute. 

During  an  attack  of  auricular  flutter  the  heart-sounds  acquire  the 
foetal  rhythm,  and  if  the  attack  be  prolonged  for  some  weeks  a  mitral 
systolic  murmur  may  develop  in  consequence  of  cardiac  dilatation. 

In  some  instances,  however,  even  when  the  ventricular  rate  exceeds 
140  or  150  beats  per  minute,  the  patient  experiences  wonderfully  little 
discomfort  beyond  slight  palpitation,  and  he  may  continue  to  lead 
an  active  life  for  several  days,  or  even  weeks,  after  the  paroxysm  of 
auricular  flutter  began.  In  such  cases  the  symptoms  may  gradually 
become  more  urgent  the  longer  the  flutter  lasts.  In  other  instances 
the  patient  may  remain  remarkably  free  from  all  urgent  symptoms  for 
many  months,  provided  he  leads  a  quiet  life.  Case  XXI.  alfords  a  good 
example. 

"When  the  auricles  are  in  flutter  the  ventricular  rate  is  usually 
one-half  of  the  auricular  rate.  The  latter  is  most  frequently  between 
250  and  300,  but  may  attain,  or  even  exceed,  a  rate  of  370  per  minute. 
In  most  instances  the  ventricular  rate  is  therefore  between  140  and  150 
per  minute,  nevertheless  a  rate  of  160  is  not  uncommon. 

"When  the  rate  of  the  ventricles  is  constantly  one-half  of  the  auri- 
cular rate,  the  ventricular  beats  and  the  arterial  pulse,  although  greatly 
accelerated,  are  rhythmic.  The  pulse  is  of  small  volume  and  may  be 
alternating  if  the  rate  exceeds  150  per  minute.  The  pulse  is  sometimes 
so  rapid  and  feeble  as  to  be  almost  imperceptible  at  the  wrist. 

Less  frequently  the  ventricular  rate  is  constantly  one-third  of  the 
auricular.  Under  these  circumstances  there  is  probably  defective  con- 
duction in  the  atrio-ventricular  bundle.  Case  XXX,,  with  an  initial 
ventricular  rate  of  only  87  per  minute,  may  be  taken  as  an  example. 
In  cases  of  this  nature  the  auricular  flutter  is  particularly  apt  to  escape 
recognition,  because  the  pulse  is  rhythmic  and  not  notably  accelerated. 

In  other  instances,  when  the  ratio  of  auricular  to  ventricular  systole 
varies  from  2:1  to  3:1,  from  2:1  to  4:1,  or  from  3:1  to  4:1,  the 
irregularity  of  the  cardiac  impulse  and  arterial  pulse  is  a  striking  feature 


84  CLINICAL  FEATUEES 

which  attracts  the  attention  of  the  physician.  Lastly,  there  may  be 
paroxysmal  attacks  in  which  the  arterial  pulse,  according  to  Mackenzie, 
attains  a  rate  of  290-300  per  minute,  and  in  Case  XXXVIIL  a  rate  of 
just  over  200  was  attained.  In  such  instances  the  auriculo-ventricular 
ratio  is  1 : 1  instead  of  2:1,  as  is  usually  the  case  during  the  initial 
stage  of  auricular  flutter. 

The  duration  of  the  paroxysmal  attacks  varies  widely  in  different 
patients  and  in  different  attacks  in  the  same  patient.  An  attack  may 
last  for  only  a  few  minutes,  for  some  hours,  or  for  several  days  or 
weeks.  Initial  attacks  are  usually  of  shorter  duration  than  subsequent 
ones.  They  may  pass  off  spontaneously.  An  attack  which  has  persisted 
for  a  day  or  two  and  caused  the  patient  much  anxiety  and  distress  may 
terminate  while  he  is  asleep.  When  he  awakens,  he  at  once  feels  that 
he  is  better.  The  palpitation,  dyspnoea,  and  precordial  discomfort  have 
vanished,  his  pulse-rate  has  fallen  from  150  or  160  to  about  80  per 
minute,  and  in  the  course  of  a  few  days  the  patient  is  able  to  get  out  of 
bed,  and  may  even  be  able  to  resume  his  former  mode  of  life  without 
experiencing  any  uneasiness  or  distress.  Once  an  attack  of  flutter  has 
occurred  there  is  a  distinct  tendency  for  attacks  to  recur  from  time 
to  time. 

II.  Auricular  Flutter  Supervening  during  the  Course  of 
Chronic  Heart  Disease 

The  majority  of  cases  of  auricular  flutter  are  included  in  this  group. 
The  patient's  history  and  physical  condition  indicate  that  he  has  been 
affected  for  many  years  with  mitral  disease  or  with  arterio-sclerosis 
and  chronic  interstitial  myocarditis.  There  may  be  co-existent 
chronic  nephritis  (Cases  XLI.  and  XLIL).  Aortic  lesions  are  seldom 
demonstrable. 

In  some  instances  the  patient,  although  affected  with  chronic 
valvular  or  myocardial  disease,  has  been  able  to  follow  his  ordinary 
mode  of  life  until  with  the  onset  of  flutter  there  arise,  suddenly  or 
insidiously,  symptoms  such  as  palpitation,  dyspnoea,  precordial  pain, 
insomnia,  and  prostration.  Sudden  attacks  of  faintness  or  of  complete 
loss  of  consciousness  may  occur  from  time  to  time  if  the  ventricular 
acceleration  becomes  extreme  (Cases  VI.,  XXXVIIL).  Bodily  fatigue, 
excessive  strain,  worry,  or  emotion,  may  be  the  immediate  cause  that 
excites  an  attack  of  flutter,  or  it  may  arise  during  some  acute  inter- 
current affection  such  as  bronchitis,  intestinal  catarrh,  or  influenza. 

On  the  onset  of  flutter,  the  patient's  condition  almost  invariably 


FLUTTEli   IN   CHRONIC   HEAHT   DISEASE  85 

becomes  worse,  much  in  the  same  way  as  so  frequently  occurs  on  the 
onset  of  auricular  librillation.  The  change  may  develop  suddenly  or 
gradually.  For  a  few  days  the  auricles  may  be  liuttering  and  the 
arterial  pulse  may  be  so  rapid  and  feeble  as  to  be  almost  imperceptible 
at  the  wrist,  and  yet  the  patient  may  be  conscious  of  no  particular 
symptoms  except  palpitation  and  some  increase  of  dyspnoea.  Within 
the  course  of  a  few  days  at  most  the  symptoms  become  more  urgent. 
The  patient  is  usually  most  comfortable  when  he  lies  propped  up  in 
bed.  The  face  acquires  a  dusky  tint,  the  liver  becomes  congested  and 
enlarged,  tenderness  is  often  developed  on  deep  pressure  over  this  organ 
in  the  right  hypochondrium  or  epigastrium,  crepitations  appear  at  the 
bases  of  the  lungs,  the  feet  may  become  oedematous,  the  complexion 
jaundiced,  and  the  urine  scanty  and  albuminous.  If  the  flutter  persists 
and  the  ventricular  rate  remains  constantly  rapid,  somnolence,  stupor, 
and  Cheyne-Stokes  respiration  may  develop.  In  other  instances  the 
patient  becomes  restless  or  even  mildly  delirious. 

The  rate  of  the  ventricles  and  of  the  arterial  pulse  depends  on  the 
rate  at  which  the  auricles  are  fluttering  and  on  the  ratio  of  auricular  to 
ventricular  systole  (2  : 1,  3  : 1,  or  4  : 1),  as  already  described.  In  most 
cases  there  is  an  initial  ratio  of  2:1,  and  the  ventricles  beat  rhyth- 
mically at  a  rate  of  about  125-160  per  minute.  In  Cases  XVIII., 
XXXYIII.,  and  XLA^I.  the  ratio  was  occasionally  1 : 1,  and  in  Case 
XVIII.  the  ventricular  rate  rose  to  290-300  per  minute.  Another 
patient,  aged  37,  whom  I  saw  with  Dr.  Edwards  of  Bridge  of  Earn,  was 
suffering  from  mitral  stenosis  and  from  auricular  flutter  that  had  come 
on  abruptly  and  had  persisted  almost  continuously  for  five  months. 
When  the  patient  was  recumbent  the  heart  was  beating  with  a  normal 
rhythm  and  at  a  rate  of  125  per  minute,  but  when  she  sat  up  in  bed  the 
rate  of  the  auricles  and  the  ventricles,  as  recorded  graphically,  rose  to 
255  per  minute. 

When  auricular  flutter  supervenes  in  a  case  of  mitral  disease  all 
the  antecedent  endocardial  murmurs  usually  become  obscured  owing  to 
the  extreme  acceleration  of  the  ventricles.  An  antecedent  mitral  pre- 
systolic murmur  will  almost  certainly  disappear.  Indeed,  it  is  almost 
impossible  to  hear  any  diastolic  murmur,  or  to  time  it  even  if  it  be 
audible,  when  the  ventricular  diastole  is  curtailed  to  0*14  second,  as  is 
the  case  when  the  ventricular  rate  is  about  150  or  160  per  minute. 
But  even  if  the  ventricular  rate  be  not  greatly  accelerated,  as  when 
it  has  fallen  to  one-fourth  of  the  auricular  rate,  a  genuine  presystolic 
murmur  can  hardly  arise,  because  when  the  auricles  are  fluttering  there 


86  CLINICAL   FEATUEES 

will  be  no  notable  rise  of  intra-auricular  pressure  during  the  last  phase 
of  ventricular  diastole  such  as  occurs  when  the  auricles  contract  once  at 
their  normal  time  in  the  cardiac  cycle. 

Auricular  flutter,  with  a  pulse-rate  of  about  150,  may  alternate 
from  hour  to  hour,  or  from  day  to  day,  with  a  physiological  rhythm  in 
which  the  rate  is  about  70-80  per  minute,  or  the  flutter  may  persist 
for  days  or  for  weeks.  In  many  instances  the  flutter  ultimately  passes 
into  auricular  flbrillation,  but  before  the  latter  is  flnally  established 
there  may  be  many  transitions  from  flutter  to  fibrillation  and  vice  versd, 
or  again  between  flutter,  fibrillation,  and  a  normal  rhythm.  During 
these  transitional  phases  it  may  be  difficult  to  determine  whether  the 
auricles  are  in  flutter  or  in  fibrillation,  especially  if  electrocardiograms 
cannot  be  obtained  or  if,  in  the  absence  of  any  long  ventriculo-diastolic 
pauses,  satisfactory  tracings  of  the  auricular  waves  in  the  jugular  pulse 
cannot  be  secured. 

After  persisting  for  several  hours,  days,  or  weeks,  the  flutter  may 
subside,  and  the  heart  regain  its  physiological  rhythm  at  a  rate  of  about 
70-80  per  minute.  '  In  all  likelihood  the  patient's  general  condition 
will  then  begin  to  improve  speedily. 

In  other  instances,  even  although  the  auricles  continue  in  flutter, 
improvement  begins  whenever  the  ventricular  rate  diminishes,  as  often 
occurs  under  the  influence  of  digitalis.  If  the  patients  continue  to  take 
this  drug  in  doses  sufficient  to  hold  the  ventricular  action  in  check, 
they  may  be  able  to  lead  a  quiet  and  fairly  comfortable  existence  for 
many  years.  In  such  cases,  however,  there  is  always  a  risk  of  sudden 
death. 

Again,  auricular  flutter  may  supervene  as  a  terminal  event  after  the 
patient  has  been  confined  to  bed,  cyanosed,  breathless  and  dropsical, 
for  many  weeks  or  months.  In  Case  III.,  for  instance,  the  patient 
had  been  suffering  for  about  nine  months  from  heart  failure  consequent 
on  mitral  disease,  and  auricular  flutter  at  a  rate  of  320  per  minute  set 
in  ten  days  before  his  death.  In  this  case  the  flutter  was  apparently 
due  to  acute  pericarditis  and  sub-acute  mitral  endocarditis  spreading 
into  the  auricular  musculature.  In  Case  VII.,  one  of  exophthalmic 
goitre  and  dilatation  of  the  heart,  the  auricles  probably  passed  into 
flutter  three  days  before  death. 

III.    AUEICULAK  FlUTTEK   WITH   PaETIAL   HeAET-BLOCK 

The  main  clinical  features  are  similar  to  those  described  in  the  pre- 
ceding group  of  cases.     Owing  to  the  existence  of  partial  heart-block. 


FLUTTER   WITH   PAKTIAL   liLOCK  87 

however,  the  rate  of  the  vontruilcs  is  less  accelerated,  and  their  rhytlim 
is  as  a  rule  irregular. 

In  the  two  preceding  groups  we  have  been  considering  cases  in 
which  the  ventricles,  at  the  onset  of  auricular  flutter,  usually  responded 
to  every  second  auricular  beat,  so  that  there  was,  for  example,  a  ratio  of 
As  :  A^s  : :  280  :  140.  In  those  cases  the  transmission  of  every  alternate 
stimulus  to  the  ventricles  was  undoubtedly  blocked.  This  blocking, 
which  is  probably  due  to  a  functional  inability  on  the  part  of  the  atrio- 
ventricular bundle  to  transmit  onwards  stimuli  at  such  a  frequent  rate, 
is  an  example  of  a  natural  protective  mechanism.  That  it  is  not  due  to 
any  pre-existing  defect  in  the  conducting  system,  as  Lewis  ^  maintains, 
is  indicated  by  the  fact  that  wlien  the  auricles  of  a  healthy  mammalian 
heart  are  set  into  flutter  experimentally  every  alternate  stimulus  to  the 
ventricles  is  likewise  blocked. 

There  are  a  few  cases  of  auricular  flutter,  however,  in  which  there 
was  apparently  a  pre-existing  pathological  depression  of  conductivity  in 
the  atrio-ventricular  bundle  whereby  the  ventricles  did  not  receive  each 
alternate  stimulus  from  the  auricles,  but  merely  every  third,  fourth, 
or  sixth  stimulus.  When  the  auriculo-ventricular  ratio  was  4 : 1  the 
ventricular  rate  was  notably  infrequent  and  the  rhythm  was  liable  to 
be  irregular.  The  defect  in  conductivity  may  have  been  latent  until  it 
was  revealed  in  consequence  of  the  auricular  acceleration. 

The  case  recorded  by  Gibson  ^  (Case  XII.)  is  a  beautiful  illustration 
of  auricular  flutter  in  association  with  partial  heart-block.  When  the 
auricles  were  beating  rhythmically  at  a  rate  of  90  per  minute,  an  occa- 
sional stimulus  to  the  ventricles  was  blocked.  When  the  auricles  were 
fluttering  at  a  rate  of  196-200  per  minute,  the  rate  of  the  ventricles 
was  usually  one-fourth  that  of  the  auricles,  and  the  ventricular  rhythm 
was  irregular.  After  death  the  atrio-ventricular  bundle  "showed  a 
very  considerable  increase  of  fibrous  tissue  with  wide  separation  of  the 
muscle  fibres  constituting  it." 

The  case  recorded  by  Hertz  and  Goodhart  ^  (Case  XIV.)  may  also  be 
referred  to  here.  In  Fig.  1  of  their  paper,  the  ventricular  beats  are 
coupled  regularly  at  a  rate  of  80  per  minute.     The  second  beat  of  each 

^  Lewis,  T.,  "  Observations  iipon  a  Curious  and  not  uncommon  Form  of  Extreme 
Acceleration  of  the  Auricle.     'Auricular  Flutter,'"  Heart.,  Lond.,  1912-13,  iv.,  171. 

2  Gibson,  G.  A.,  "A  Discussion  on  some  Aspects  of  Heart-block,"  Brit.  Med. 
Joiirn.,  Lond.,  1906,  ii.,  1113. 

3  Hertz,  A.  F.,  and  Goodhart,  G.  ^Y.,  "  The  Speed-limit  of  tlie  Human  Heart," 
Quart.  Journ.  of  Med.,  Oxford,  1908-9,  ii.,  213. 


88  CLINICAL   FEATUEES 

couple  is  so  premature  as  to  give  the  impression  of  being  a  ventricular 
extrasystole.  Consequently,  the  ventricles  responded  to  supra-ventri- 
cular stimuli  only  40  times  per  minute,  and  as  the  auricular  rate  was 
240  per  minute  there  was  a  ratio  of  As  :  Vs  : :  6  : 1,  which  suggests  that 
the  conductivity  of  the  atrio-ventricular  bundle  was  probably  defective. 
The  defect  may  have  been  due  to  vagus  stimulation  or  to  drug  adminis- 
tration, however,  and  not  to  structural  changes  in  the  atrio-ventricular 
bundle,  for  the  ventricular  rate  rose  to  170  after  an  injection  of  5^  grain 
of  atropin. 

IV.  AuEicuLAE  Flutter  in  Association  with  Complete  Atrio- 
ventricular Heart-block 

Whenever  there  is  a  lesion  severing  completely  the  main  stem  of 
the  atrio-ventricular  bundle  the  ventricular  rhythm  becomes  wholly 
dissociated  from  that  of  the  auricles.  The  ventricles  beat  with  an 
independent  rhythm  in  response  to  stimuli  coming  from  the  atrio- 
ventricular bundle  below  the  lesion.  The  auricular  beats  may  be 
slow  or  fast,  regular  or  irregular,  strong  or  weak,  yet  the  rate,  rhythm, 
and  strength  of  the  ventricular  beats  are  wholly  independent  of  the 
auricles.  Moreover,  the  vagus  and  sympathetic  influences  that  retard 
or  accelerate  the  auricles  in  no  wise  affect  the  ventricles.  The  ventri- 
cular rate  is  slow,  usually  30-.36  per  minute,  the  rhythm  is  usually 
absolutely  regular,  and  the  contractions  are  not  necessarily  enfeebled. 
Numerous  cases  have  been  reported  in  which,  during  life,  exact  records 
of  complete  atrio-ventricular  dissociation  were  obtained,  and  post- 
mortem the  main  stem  of  the  bundle  was  found  to  be  severed. 

One  notable  case  of  this  nature  was  recorded  by  Gibson  and  myself^ 
in  1909.  In  another  case  that  had  been  under  my  own  observation  and 
in  four  similar  cases  recorded  by  P.  Macdiarmid,^  I  found  the  main 
stem  of  the  atrio-ventricular  bundle  severed  by  chronic  inflammatory 
lesions. 

Experimental  and  clinical  observations  indicate  that  unless  the 
heart  is  under  the  influence  of  vagus  stimulation,  partial  severance 
of  the  bundle  does  not  cause  complete  heart-block.  On  the  other 
hand,  the  block  may  have  been  complete  during  life,  and  yet  no  lesion 
can  be  discovered  in  the  bundle.     Only  one  case  of  this  nature  (Fig.  73) 

1  Gibson,  G.  A.,  and  Ritchie,  W.  T.,  "A  Historic  Instance  of  the  Adams-Stokes 
Syndrome  due  to  Heart-block,"  Edin.  Med.  Journ.,  1909  (N.S.)  ii.,  315,  507. 

2  Macdiarmid,  P.,  Heart-block  and  Adams-Stokes  Disease,  Thesis,  University  of 
Edin.,  1911. 


FLUTTER   WITH   COMPLETE   BLOCK  89 

has  come  under  my  notice.  After  a  typical  Adams-Stokes  seizure  in 
a  man  aged  7"",  the  l)lock  remained  complete  for  the  two  and  a  half 
months  during  which  the  }»atient  was  under  observation,  and  it  was 
not  relieved  by  atropin.  A  fortnight  after  the  patient  was  last  seen, 
he  died  suddenly.  Both  nodes,  the  bundle,  and  the  initial  parts  of  both 
its  branches,  were  examined  in  serial  sections,  but  no  lesion  could  be 
detected.  The  true  cause  of  the  heart-block  was  not  elucidated  until 
Miss  Meiklejohn,  to  whom  I  am  indebted  for  the  examination  of  this 
heart,  made  serial  sections  of  the  inter-ventricular  septum  below  the 
level  of  the  pars  membranacea  septi.     It  was  then  found   that  both 


iliilllllllliilllll  I IllilUlllllllllllllllllilllllilll 


Fig.  73. — Coniiil'-ti'  li^'art-lilock,  with  an  auricular  rate  of  07  and  a  ventricular  rate  ol'Ss  per  minute. 
Derivation  I.     1  cm.  =  l  millivolt. 

branches  of  the  bundle  were  almost  wholly  obliterated  by  dense  fibrous 
tissue. 

The  only  recorded  instance  of  auricular  flutter  in  association  with 
complete  heart-block  is  Case  I.  (p.  35).  Antecedent  to  the  onset  of 
flutter  there  was  complete  heart-block,  with  auricular  and  ventricular 
rates  respectively  of  50-60  and  31-35  per  minute.  The  onset  of 
auricular  flutter  at  a  rate  of  273  per  minute  did  not  disturb  the 
rate,  rhythm,  or  strength  of  the  ventricular  beats,  and  the  patient 
was  unaware  of  any  fresh  symptoms.  This  case  demonstrates  clearly 
that  the  symptoms  associated  with  auricular  flutter  are  not  due  to  the 
flutter  directly,  but  arise  indirectly  as  a  result  of  the  great  ventricular 
acceleration  in  response  to  the  flutter. 


CHAPTEE  VI 

GEAPHIC   EECOEDS 

When  the  auricles  are  in  flutter,  their  contractions  can  often  be 
recorded  graphically.  As  characteristic  tracings  and  electrocardio- 
grams have  already  been  considered  in  Chapter  IV.,  only  the  salient 
features  need  be  referred  to  here. 

(1)  SjDhygmograms. — The  rate  and  rhythm  of  the  arterial  pulse  vary 
greatly  in  different  cases  and  at  different  times  in  any  one  case.  When 
the  ventricular  rate  is  constantly  one-half  of  the  auricular  rate,  the 
record  is  that  of   a  rhythmic   rapid   pulse   at   a   rate  of    about   130- 


FiG.  74. — Spliygraograms  in  auricular  flutter  (Case  II.).  In  a  the  ventricles  are  responding  to  every  second 
auricular  beat,  and  the  pulse  is  frequent  and  alternating.  In  6  the  ventricles  are  responding  to  every 
fourth  auricular  beat. 

160  per  minute  (Fig.  74,  a).  The  pulse  is  often  alternating  and  may 
be  hyperdicrotic. 

When  the  ventricles  respond  uniformly  to  every  third  or  every 
fourth  auricular  beat,  the  arterial  tracings  do  not  necessarily  differ 
in  any  essential  respect  from  the  normal  (Pig.  74,  l),  although  when 
the  auriculo- ventricular  ratio  is  3  : 1  the  pulse  may  be  alternating,  as  in 
Case  XXXII. 

If  the  ventricles  are  responding  irregularly  to  fluttering  auricles, 
the  arterial  pulse  tracing  is  at  first  sight  wholly  irregular.  But  when 
the  tracing  is  analysed,  it  will  usually  be  found  that  the  pulse-beats 
occur  in  groups  of  uniform  duration,  representing  multiples  of  the  inter- 
auricular  period.  This  is  illustrated  in  Fig.  75.  These  records  were 
obtained  from  a  ploughman,  aged  39,  who  had  been  suffering  for  four 
months  from  breathlessness  and  weakness,  and  who  had  been  unfit 
for  any  work  for  three  weeks.  No  history  of  acute  rheumatism  or 
syphilis  could  be  elicited.  When  admitted  to  the  Eoyal  Infirmary 
under  the  care  of  Dr.  Lovell  Gulland,  the  patient  was  greatly  troubled 


SPlIVdMOClLVrillC    lIKCOIiDS  91 

with  breatlilessness  and  cough,  the  face  was  dusky  with  an  icteric  tint, 
the  feet  and  hmgs  were  (edematous,  the  Hver  was  enlarged,  and  pressure 
over  it  ehcited  tenderness.  The  heart  was  moderately  enlarged,  but  no 
murmurs  were  audible.  The  ventricles  were  beating  at  a  rate  of  140- 
IGO  per  minute;  the  rhythm  was  usually  irregular,  as  in  Fig.  75,  but 


' le u ^o 1 

Fio.  ~j. — Spliygmo^Tams  from  a  case  of  auricular  flutter  with  irregular  ventricular  responses  and 
grouping  of  the  arterial  beabi. 

at  times  the  pulse  was  rhythmic,  and  it  was  then  alternating.     The 
auricles  were  probably  in  flutter  at  a  rate  of  about  320  per  minute. 

Digitalin  was  administered,  and  ten  days  later,  when  electrocardio- 
grams could  be  recorded,  the  auricular  deflexions,  which  were  either 
irregular  or  regular  at  a  rate  of  380  per  minute,  represented  either 
a  coarse  fibrillation  or  a  form  of  auricular  action  with  simultaneous 
flutter  and  fibrillation.     One  week  later,  when  the  ventricles  were  beat- 


][■/]!    »     'J    \^\j     v'     1/     i/^,,y^/'       '1/     1/     1; 


\\  2.        Z    ^  2.         2. 


Fig.  7ti. — Auricular  flutter.    Jugulo-carotid  and  brachial  tracing's  showing  a  ventricular  response  to 
every  second  or  every  third  auricular  beat. 

ing  slowly  and  irregularly,  the  auricular  deflexions  were  of  small  size, 
irregular  form  and  frequency,  indicating  auricular  fibrillation.  When 
the  patient  left  hospital  two  months  later,  his  general  condition  was 
greatly  improved. 

Another  example  of  irregular  ventricular  responses  in  flutter  is 
shown  in  Fig.  76  from  Case  II.  The  ventricles  were  usually  respond- 
ing to  each  alternate,  but  occasionally  to  every  third,  auricular  beat. 
After  the  latter  event  there  was  a  transient  but  well-marked  pulsus 


92 


GEAPHIC   KECORDS 


alternans.  The  irregularity  of  the  pulse  in  this  instance  was  therefore 
due  to  the  ventricles  responding  irregularly  to  rhythmic  auricular  beats, 
and  also  to  the  delay  of  the  smaller  pulse  waves  when  alternation 
developed.      This  delay  can  also  be  demonstrated  by  comparing  the 


Fig.  77.  — Jugulo-earotid  and  brachial  tracings.  Auricular  flutter  at  a  rate  of  196  per  minute.  Successive 
ventricular  beats  are  responses  to  every  third,  tifth,  and  sixth  auricular  beats.  Case  XII.,  9th  February 
190(3.    The  time  record  is  0'2  second. 

interval  between  each  deflexion  B  in  an  electrocardiogram  with  the  • 
corresponding  pulse  wave  in  a  sphygmogram  recorded  simultaneously 
(Plate  XXI.,  Pig.  106). 

The  irregularity  of  the  arterial  pulse  may  be  intensified  still  further 
by  ventricular  beats  failing  to  open  the  aortic  valve  and  consequently 


Fig.  78.— Auricular  flutter  at  a  rate  of  260  per  minute.     The  ventricles  respond  to  eveiy  fourth  auricular 
beat.    Jugulo-earotid  and  brachial  tracings  (Case  II.). 

having  no  representative  in  the  sphygmogram  (Plate  XXL,  Pig.  106),  and 
also  by  the  occurrence  of  ventricular  extrasystoles  (Plate  XV.,  Pig.  83). 
2.  Jugulo-earotid  Tracings. — When  the  rate  of  the  ventricles  is 
infrequent  and  does  not  attain  one-quarter  of  the  auricular  rate,  the 
tracings  usually  present  large,  rhythmic  auricular  waves  during  each 
ventricular  diastole  (Pigs.  31  and  77).  During  ventricular  systole  the 
auricular  waves  may  be  obscured  by  the  waves  c  and  v,  but  in  some 


PLATE   XIV. 


Fig.  79.— Auricular  Mutter.     The  ventricular  v;\{f  is  oii'-liall  tliat  ol'  tlif  am  iclos.     Case  II. 
Derivation  II.     1  cm.  =  l  millivolt.     {Edin.  Mai.  Journ.,  1912,  vol.  ix.) 


\f^  ^s/n/^' A/v^/\;v' aAT"  a 


.iiiiiiiiiiiiiuiiiiiiuuituiiiiniiiiiiiiiuiiiiiiiiiiiiiiiiiiiuiuiiiui 

Fig.  80.— Auricular  flutter.     The  ventricular  rate  i.s  one-third  that  of  the  auricles.     Case  XLVII. 
Derivation  II.     1-5  em.  =  1  millivolt.    (G.  D.  Mathewson.)    {Edin.  Med.  Jo^lrn.,  1913,  vol.  xi.) 


I^J^iSJ^isJsH^ 


laiiiiiiiinuiiiuiuuiuiuaiiiinimiiuumiiiiiuuiuuiimuiiiiiuuitiiiiuiiiuuiuiiiuiuiiiiiiiiiiuiuunumi 


I'li;.  SI. — Auricular  flutter.     The  ventricular  rate  is  one-fouith  that  of  the  auricles.     Case  II. 
Derivation  II.    1  cm.  =  I  millivolt.    {Edin.  Med.  Journ.,  I'.il2,  vol.  ix.) 


ELECTKOCAIIDIOGUAMS  93 

instances  the  auricular  waves  occurring  during  ventricular  systole  are 
larger  than  those  during  ventricular  diastole  (Fig.  77),  because  during  the 
former  phase  the  tricuspid  orifice  is  closed  and  during  the  latter  open. 

If  the  auricles  are  beating  uniformly  four  times  as  fast  as  the 
ventricles,  the  four  auricular  waves  for  each  arterial  pulse-beat 
(Fig.  78)  must  not  be  mistaken  for  a,  c,  v,  and  h  waves  of  a  normal 
rhythm  (see  p.  7).  If  the  auriculo-ventricular  ratio  is  constantly  3 : 1, 
the  three  waves  in  the  jugular  curve  may  simulate  a,  c,  and  v  waves  of 
a  normal  rhythm  (see  p.  112). 

When  the  auricular  rate  is  uniformly  twice  that  of  the  ventricles,  the 
jugular  pulse  is  of  the  ventricular  form — the  curve  rises  with  the  onset 
of  ventricular  systole,  and  after  a  more  or  less  well-marked  systolic 
plateau,  falls  when  the  tricuspid  valve  opens  (Figs.  43,  51,  and  72). 

If  the  ratio  of  As :  Ys  is  irregular,  the  form  of  the  jugulo-carotid 
tracing  is  inconstant,  being  of  the  ventricular  form  when  the  ventricles 
respond  to  every  alternate  auricular  beat,  and  presenting  definite 
auricular  waves  during  each  of  the  prolonged  ventricular  diastoles. 

3.  Electrocardiograms. — The  UMricular  deflexions  are  rhythmic,  and 
usually  occur  at  a  rate  of  about  200-320  per  minute.  The  maximum 
rate  in  my  own  cases  was  377  per  minute  (Case  \.),  but  in  one  of 
Hume's  cases  (Case  XLIV.)  the  rate  was  probably  about  500  per  minute. 
In  each  individual  case  the  deflexions  are  not  merely  rhythmic,  but  as 
recorded  by  each  derivation  are  almost  invariably  of  constant  form, 
except  in  so  far  as  they  may  be  distorted  by  ventricular  deflexions. 
By  derivation  I.  (right  hand  and  left  hand)  the  deflexions  are  mono- 
phasic  and  of  comparatively  small  amplitude.  They  may  indeed  be  so 
small  as  to  be  almost  imperceptible,  as  in  Case  III.  By  derivations  II. 
(right  hand  and  left  foot)  and  III.  (left  hand  and  left  foot),  they  are 
larger  and  often  diphasic  (Plate  IX.),  with  the  initial  deflexion  upwards. 
The  auricular  beats  usually  succeed  one  another  so  rapidly  that  when 
one  auricular  deflexion  ends  another  begins  (Plate  XIV.). 

In  their  diphasic  form  the  auricular  deflexions  representing  flutter 
difier  from  the  normal,  and  correspond  with  those  that  may  be  observed 
when  the  auricles  are  under  vagus  inhibition.  This  abnormal  (diphasic) 
form  probably  signifies  that  the  auricular  contractions  are  initiated  at 
some  site  other  than  the  normal  one. 

If  the  auricular  deflexions  vary  somewhat  in  form,  size,  and  rhythm, 
and  yet  their  rate  does  not  exceed  about  370  per  minute,  the  auricular 
action  is  probably  a  combination  of  flutter  and  fibrillation  (Fig.  83). 
In  true  fibrillation  the  auricular  deflexions  are  small,  irregular  in  size 


94  GRAPHIC   RECORDS 

and  rhythm,  and  occur  at  a  rate  of  usually  380-520  per  minute.  In 
Case  V;  gradual  transitions  from  auricular  fibrillation  to  flutter  were 
recorded  (see  Plate  XXL),  and  similarly  in  the  case  described  by 
Canby  Robinson^  flutter  and  fibrillation  alternated  with  each  other 
several  times.  In  this  case  the  auricles  were  fluttering  at  a  rate  of 
380  per  minute,  while  the  ventricular  beats  were  rhythmic  at  a  rate 
of  95  per  minute.  The  ventricular  beats  then  became  arrhythmic  and 
no  definite  correlation  could  be  determined  between  the  auricular  and 
the  ventricular  beats,  probably  because  the  auricular  activity  was  a 
combination  of  flutter  and  fibrillation.  A  few  minutes  later  the 
electrocardiogram  was  characteristic  of  auricular  fibrillation. 

The  ventricular  deflexions  in  cases  of  auricular  flutter  are  of  such 
form  as  indicates  supra-ventricular  stimulation.  The  amplitude  of  the 
individual  deflexions  Q,  B,  S,  and  T  varies  in  different  cases  according 
to  the  nature  of  the  valvular  lesion  and  the  predominance  of  hyper- 
trophy in  right  or  left  ventricle.  For  example,  in  Case  III.,  with  mitral 
stenosis,  B  is  larger  by  derivation  III.  than  by  derivation  I.,  whereas  8 
is  larger  by  derivation  I.  than  by  derivation  III.  In  Case  I.,  however, 
with  predominant  hypertrophy  of  the  left  ventricle,  B  is  larger  by 
derivation  I.  than  by  derivation  III.,  while  S  is  larger  by  derivation 
III.  than  by  derivation  I.  (see  Plates  IX.  and  XL). 

When  the  ventricular  rate  is  extremely  high,  not  only  is  ventricular 
diastole  curtailed  to  about  one-third  of  its  normal,  but  the  duration  of 
ventricular  systole  is  also  shortened.  Thus  in  Case  II.,  with  a  ventri- 
cular rate  of  141-5  per  minute,  ventricular  systole  lasted  about  0'245 
second  as  against  the  normal  0'30  second. 

1  Robinson,  G.  Canby,  "  The  Relation  of  the  Auricular  Activity  following 
Faradization  of  the  Dog's  Auricle  to  Abnormal  Auricular  Activity  in  Man,"  Journ. 
ofExix  Med.,  New  York,  1913,  xviii.,  704. 


PLATE   XV. 


,^  ^/y\\  /VV|^N\V*  1^"  f^^H^  [J^  i^jsS^  N 


Fig.  S2. — Auricular  flutter  at  a  rate  of  ijd-i  per  minute,  with  irregular  ventricular  resiJonse.s. 
Case  II.  (22nd  August  11112).     Derivation  II.     1  cm.  =  1  millivolt. 


Q  Sk     ^ 

iiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiniiiiiiiiiiiiiiiiiiiiiilillllilllllitlllilillliiiiiiiiiiiiiiinni 

Fig.  S3.  —Auricular  flutter  and  tibrillation  combined.    One  ventricular  beat  (&)  is  an  extrasystole.    Brachial  pulsations 
and  electrocardiogram  by  derivation  III.    Case  V.     lcm.  =  l  millivolt.     {Quart.  Journ.  Med.,  \ol.vn.) 


CHAPTER   VII 

THE   ACTION   OF  THE   VAGUS   AXD   SYMPATHETIC 

The  rate  of  stimulus  production,  the  excitability,  contractility,  con- 
ductivity, and  tone  of  the  heart,  may  be  influenced  by  many  factors, 
and  notably  by  those  of  nervous  origin. 

Chronotropic  influences  are  expressed  by  changes  in  the  rate  of 
stimulus  production.  This  may  be  accelerated  (positive  chronotropic 
effect)  or  retarded  (negative  chronotropic  effect).  Bathmotropic  influences 
are  those  upon  the  excitability  of  the  heart  muscle ;  positive  bathmo- 
tropic influences  increase,  whereas  negative  bathmotropic  influences 
lower,  its  excitability.  Dromotropic  influences  are  those  upon  con- 
ductivity within  the  heart,  and  are  most  evident  upon  the  atrio- 
ventricular bundle  system.  Positive  and  negative  dromotropic 
influences  respectively  improve  and  impair  the  conduction  of  stimuli. 
Inotropic  infl^iences  are  expressed  by  increase  or  decrease  of  contrac- 
tility. They  may  be  positive  or  negative  according  as  the  contraction 
of  muscle  fibres  is  strengthened  or  weakened.  Tonotropic  influences 
are  those  affecting  the  tone  of  the  heart-muscle ;  when  positive  they 
heighten,  when  negative  they  lower  the  muscle  tone. 

The  effects  of  each  of  these  influences  may  be  primary  or  secondary, 
and,  as  pointed  out  by  Wenckebach,^  they  are  often  of  complex  nature. 
Thus  a  j)rimary  negative  chronotropic  influence  lessening  the  rate  of 
the  auricles  may  cause  secondary  dromotropic  and  inotropic  effects,  as 
revealed  by  improved  conduction  of  stimuli  and  stronger  contractions. 
Again,  a  primary  negative  dromotropic  influence  on  the  auricles,  causing 
blocking  of  stimuli  within  their  walls,  may  cause  a  secondary  negative 
inotropic  effect,  which  is  manifested  by  weakening  of  the  beats. 

In  order  to  appreciate  correctly  the  action  of  the  vagus  and 
sympathetic  on  the  heart  when  the  auricles  are  fluttering,  it  is 
necessary  to  understand  the  effects  on  hearts  with  a  physiological 
rhythm. 

1  "Wenckebach,  K.  F.,  Die  Arhijthmie  als  Ausdruck  bestimmter  Funktionsstorungen 
des  Herzens,  Leipz.,  1903,  134. 

95 


96     THE   ACTION   OF   THE   VAGUS   AND   SYMPATHETIC 


I.  The  Action  of  the  Vagus  on  the  Heakt  Beating  with  a 
Physiological  liHYTHM 

The  striking  effects  of  the  vagus  on  the  normal  mammalian  heart, 
as  recorded  by  MacWilliam/  Eoy  and  Adami,^  Bayliss  and  Starling,^ 
Gaskell,^  Engelmann;5  Hering,''  Einthoven/  and  other  investigators,  are 
well  known.  Kecent  experimental  work  on  animals  suggests  that  the 
richt  vagus  exerts  its  influence  especially  on  the  sinus  node  and  the 
auricles,  whereas  the  left  vagus  has  a  preponderant  influence  on  the 
atrio- ventricular  conducting  system  and  the  ventricles,  but  it  is  doubtful 
whether  this  holds  good  for  the  human  heart. 

The  vagus  effects  on  the  human  heart,  originally  studied  by 
Czermak,^  have  been  described  by  Eobinson  and  Draper  ^  and  by 
myself,^*^  and  have  been  shown  to  be  comparable  to  those  on  the 
lower  mammalian  heart.  Stimulation  of  the  vagus — right  or  left — 
may  be  effected  by  means  of  digital  compression  upon  the  nerve  in 
the  neck,  whereas  the  vagus  endings  in  the  heart  can  be  paralysed  by 
the  subcutaneous  injection  of  0-02-0-03  grain  of  atropin  sulphate  given 
subcutaneously. 

1  MacWilliam,  J.  A.,  "  On  the  Phenomena  of  Inhibition  in  the  Mammalian 
Heart,"  Journ.  of  Phijsiol.,  Camb.,  1888,  ix.,  345. 

2  Roy,  C.  S.,  and  Adami,  J.  G.,  "Contributions  to  the  Physiology  and  Pathology 
of  the  Mammalian  Heart,"  Philos.  Trans.  Roy.  Soc.  Lond.,  B,  1893,  clxxxiii.,  199. 

3  Bayliss,  W.  M.,  and  Starling,  E.  H.,  "  On  some  Points  in  the  Innervation  of  the 
Mammalian  Heart,"  Journ.  of  PhijsioL,  Camb.,  1892,  xiii.,  407. 

■i  Gaskell,  W.  H.,  "  On  the  Rhythm  of  the  Heart  of  the  Frog,  and  on  the  Nature 
of  the  Action  of  the  Vagus  Nerve,"  Philos.  Trans.  Eoy.  Soc.  Lond.,  1882,  clxxiii.,  3,  993 ; 
*'  The  Nature  of  the  Action  of  the  Cardiac  Nerves,"  Schcifer's  Text-book  of  Physiology, 
Edin.  and  Lond.,  1900,  ii.,  203-221. 

5  Eno-elmann,  Th.  W., "  Ueber  die  Wirkungen  der  Nerven  auf  das  Herz,"  Arch.  f. 
Anat.  u.  Physiol.  (Physiol.  Abt.),  Leipz.,  1900,  315. 

6  Hering,  H.  E.,  "  Ueber  die  unmittelbare  Wirkung  des  Accelerans  und  Vagus 
auf  automatisch  schlagende  Abschnitte  des  Stiugethierherzens,"  Arch.f  d.ges.  Physiol, 
Bonn,  1905,  cviii.,  281  ;  "  Experimentelle  Studien  an  Saugethieren  iiber  das  Elektro- 
kardiogramm,"  ibid.,  1909,  cxxvii.,  155. 

"  Einthoven,  W.,  and  Wieringa,  J.  H.,  "  Ungleichartige  Vaguswirkungen  auf 
das  Herz,  elektrokardiographisch  untersucht,"  Arch.  f.  d.  ges.  Physiol,  Bonn,  1913, 
cxlix.,  48. 

8  Czermak,  J.  N.,  "  Ueber  mechanische  Reizung  des  Nervus  vagus  beim 
Menschen,"  Gesammelte  Schriften,  Leipz.,  1879,  i.,  2,  779. 

9  Robinson,  G.  Canby,  and  Draper,  G.,  "  Studies  with  the  Electrocardiograph  on 
the  Action  of  the  Vagus  Nerve  on  the  Human  Heart,"  Journ.  of  Ex]}er.  Med.,  New- 
York,  1911,  xiv.,  217. 

10  Ritchie,  AV.  T.,  "  The  Action  of  the  Vagus  on  the  Human  Heart,"  Quart.  Journ. 
of  Med.,  Oxford,  1912-13,  vi.,  47. 


PLATE    XVI. 


THE   ACTION   OF   THE   VAGUS  97 

1.  Effects  on  the  Auuicles 

I.  Rate.  —  (1)  Compression  of  the  vcif/us  may  lengthen  auricular 
diastole  and  thus  retard  the  rate  of  the  whole  heart.  The  degree  of 
auricular  retardation  thus  induced  varies  considerably  in  different 
individuals,  but  the  right  vagus  is  almost  invariably  more  effective  than 
the  left.  A  pronounced  retardation  of  the  whole  heart  by  means  of 
compression  of  the  right  vagus  in  shown  in  Eig.  84,  obtained  l^y  deriva- 
tion II.  from  a  man  aged  40.  Before  vagus  compression,  the  duration  of 
auricular  diastole  was  0"80-0'84  second,  whereas  the  longer  of  the  two 
auricular  diastoles  during  the  compression  period  lasted  2*31  second. 
A  still  more  pronounced  inhibition  of  the  whole  heart  is  shown  in  Fig. 


;4>j-''" 


D.M,  62. 


Fig.  Sij. — Diagram  showing  auricular  acceleration  after  0'0-2  grain  of 
atropin  sulphate.  The  ventricular  rate  is  not  increased.  From  a 
case  of  complete  heart-block.    {Quart.  Joura.  Med.,  vol.  \i.) 

85,  where  compression  of  the  right  vagus  caused  standstill  of  the  heart 
for  4'44  seconds.  Similar  effects  in  the  human  heart  have  been  recorded 
by  Wenckebach,^  Laslett,-  and  others,  and  in  the  dog's  heart  by 
Einthoven,^  and  Eothberger  and  Winterberg.^ 

(2)  Atrojnn  paralyses  the  vagus  endings  in  the  heart,  and  thus 
accelerates  the  auricles.      This  effect  is  shown  in  Figs,  86  and  87.      The 

1  Wenckebacli,  K.  F.,  "  Beitriige  zur  Kenutnis  der  menschliclien  Herztiitigkeit," 
Arch.f.  Anat.  u.  Physiol.  (Physiol.  Abt.),  Leipz.,  1908,  Suppl.,  5,3. 

^  Laslett,  E.  E.,  "  Syncopal  Attacks,  a.ssociated  with  Prolonged  Arrest  of  the 
Whole  Heart,"  Qimrt.  Joura.  of  Med.,  Oxford,  1908-9,  ii.,  347. 

2  Einthoven,  W.,  "  Le  telecardiogranime,"  Arch,  intermit,  de  Physiol,  Liege, 
1906-1907,  iv.,  132. 

*  Rothberger,  C.  J.,  and  "Winterberg,  H.,  "  L'eber  die  Beziehungen  der  Herznerven 
zur  automatischen  Reizerzeugung  und  zum  plotzlichen  Herztode,"  Arch.  f.  d.  ges. 
Physiol,  Bonn,  1911,  cxli.,  343. 

17 


98     THE    ACTION   OF   THE   VAGUS   AND    SYMPATHETIC 

curves  in  Fig.  86  were  constructed  from  a  continuous  record  taken  from 
a  man,  aged  62,  who  presented  complete  heart-block.  The  auricular  rate 
was  87*5  per  minute  before  the  drug  was  given.  Twenty  minutes  after 
the  subcutaneous  injection  of  0*02  grain  of  atropin  sulphate  the  auricular 
rate  had  risen  to  101  per  minute,  but  the  ventricular  rate  did  not 
become  accelerated.  A  pronounced  initial  retardation,  followed  by 
acceleration,  is  shown  in  Fig.  87  from  a  man,  aged  45,  presenting  digitalis 
heart-block.  Before  the  test  was  performed  the  auricular  rate  varied 
from  83-85  per  minute.  The  subcutaneous  injection  of  0'03  grain  of 
atropin  sulphate  caused  an  initial  retardation  of  auricular  rate  to  75  per 
minute.     This  passed  off  at  the  end  of  seven  minutes,  and  was  followed 

(2     13  15  17    JliIj  psii. 


«  J.C,  45. 

I'lG.  87. — Diagram  to  show  the  rate  per  minute  of  auricles,  A,  and  of  ventricles,  V,  and  the 
a-G  interval  before  and  after  0-03  grain  of  atropin  sulphate  in  a  case  of  digitalis  heart- 
block.     (Quart.  Journ.  Med.,  vol.  vi.) 

by  a  progressive  acceleration  attaining  a  maximum  of  107  per  minute 
twenty  minutes  after  injection  of  the  drug.  From  the  twenty-first 
until  the  thirty-seventh  minute  an  auricular  rate  of  101-107  was 
maintained,  rising  to  120  when  the  patient  rose  up  from  the  couch  at  the 
forty-second  minute. 

II.  Excitability. — (1)  Compression  of  Vagus. — Physiologists  have  de- 
monstrated that  excitation  of  the  vagus  in  animals  depresses  the  excit- 
ability of  the  auricular  muscle  (primary  negative  bathmotropic  effect). 
Gaskell^  states  that  this  effect  "is  now  universally  allowed."  It  is 
difficult  to  estimate  the  excitability  of  the  auricular  muscle  in  man, 
because  the  methods  applied  by  the  physiologist  to  determine  the  thres- 

1  Gaskell,  W.  H.,  "  The  Contraction  of  Cardiac  Muscle,"  Schclfer's  Text-book  of 
Physiology,  Edin.  and  Lend.,  1900,  ii.,  204. 


THE   ACTION  OF   THE   VAGUS  99 

hold  of  excitability  are  not  applicable  to  the  human  heart.  The  only 
criterion  which  permits  the  clinician  to  assume  that  the  excitability 
of  the  human  auricle  is  increased  is  the  occurrence  of  supra-ventricular 
ex trasy stoles,  and  even  these  indicate  the  presence  of  one  or  more 
unduly  irritable  foci  in  the  auricular  wall  rather  than  of  a  general 
increase  of  excitability  throughout  the  auricular  muscle.  An  increased 
rate  of  auricular  contraction  is  still  less  reliable  evidence  of  heightened 
auricular  excitability,  because  acceleration  of  rate  may  be  due  to  other 
causes ;  for  example,  quicker  rate  of  stimulus  production,  or  shortening 
of  the  refractory  phase. 

In  my  own  observations  on  the  human  heart  I  have  never  observed 
any  indication  of  auricular  excitability  being  increased  or  depressed 
during  compression  of  either  vagus. 

(2)  Atropin. — As  vagus  stimulation  in  animals  depresses  auricular 
excitability,  it  might  be  expected  that  atropin,  by  cutting  off  the  vagus 
influences,  would  increase  excitability.  The  drug  might  therefore  be 
expected  to  promote  the  onset  of  supra-ventricular  extrasystoles,  but 
I  have  never  observed  this  effect  in  man. 

III.  Contractility. — Physiologists  are  agreed  that  depression  of  auri- 
cular contractility  is  an  early  and  striking  effect  of  vagus  stimulation 
and  that  the  onset  of,  and  recovery  from,  depression  of  contractility  are 
usually  gradual.  Although  the  height  of  the  summit  P  is  not  neces- 
sarily proportionate  to  the  strength  of  auricular  systole,  we  know  that 
this  deflexion  is  increased  when  the  auricles  are  hypertrophied,  or  when 
both  vagi  have  been  cut.  Einthoven^  has  demonstrated  that  in  the 
dog  during  vagus  stimulation  the  deflexion  P  may  be  diminished  in  size 
and  become  diphasic.  Similar  observations  have  been  recorded  in  the 
dog's  heart  by  Kahn,^  Kothberger  and  Winterberg,^  and  others.  My 
own  observations  on  the  human  heart  demonstrate  the  same  effects. 
One  record,  from  a  man  aged  55,  suffering  from  mitral  stenosis  and  pre- 
senting a  loud,  rough  presystolic  murmur,  showed  that  compressiojKbf  the 
left  vagus,  although  retarding  the  rate  of  the  heart  very  slightly,  caused 
a  notable  reduction  in  the  amplitude  of  the  auricular  deflexions.  This 
may  probably  be  regarded  as  indicating  depression  of  auricular  con- 
tractility.    In  Eig.  84  right  vagus  compression  reduced  the  amplitude 

1  Eintlioven,  "W.,  "Weiteres  liber  das  Elektrokardiogramm,"  Arch.  f.  d.  ges. 
Physiol,  Bonn,  1908,  cxxii.,  517. 

2  Kalin,  E.  H.,  "  Elektrokardiogrammstudien,"  ibid.,  1911,  cxl.,  627. 

2  Rotliberger,  C.  J.,  and  Winterberg,  H.,  "Ueber  die  experinientelle  Erzeugung 
extrasystolisclier  ventiikuliirer  Tacliykardie  durcli  Acceleransreizung,"  ibid.,  1911, 
cxlii.,'461. 


100     THE   ACTION   OF   THE   VAGUS   AND    SYMPATHETIC 

of  the  auricular  deflexions  and  retarded  the  whole  heart.  In  Fig.  88 
the  auricular  deflexions  P3  and  P4  became  of  abnormal  form.  In 
view  of  Lewis's  ^  experimental  researches  on  the  form  of  the  auricular 
deflexion  associated  with  primary  negativity  in  different  parts  of  the 
auricle,  the  inhibitory  effect  in  Fig.  88  was  probably  most  pronounced 
at  the  sinus  node,  and  during  the  period  of  vagus  compression  some 
other  part  of  the  auricle  initiated  the  stimulus  for  contraction. 

(2)  Atropin. — After  section  of  both  vagi  in  dogs,  the  height  of  the 
deflexion  P,  as  demonstrated  by  Einthoven,^  is  increased  nearly  three- 
fold. It  might  therefore  be  expected  that  atropin  would  increase  the 
contractility  of  the  human  auricles,  but  I  have  not  observed  this  effect. 
Their  contractility  may  possibly  be  increased  and  yet  the  change  be 
masked  owing  to  the  acceleration  of  rate. 

IV.  Conductivity. — That  vagus  stimulation  may  depress  conductivity 
in  the  auricular  walls  was  shown  experimentally  by  GaskelF  and 
MacWilliam.^  This  change  in  the  human  heart,  when  slight,  probably 
results  in  undue  prolongation  of  auricular  systole,  and,  when  pronounced, 
in  auricular  fibrillation.  Einthoven  ^  has  recorded  the  former  effect  in 
the  dog,  and  Fig.  88  shows  it  in  the  human  heart.  In  this  figure  the 
deflexions  P3  and  P4  last  0"245  and  0*280  second  respectively,  as  com- 
pared with  0"105  second  in  the  case  of  P8  after  withdrawal  of  vagus 
compression. 

We  know  that  vagus  stimulation  depresses  auricular  conductivity 
and  promotes  the  onset  of  auricular  fibrillation.  Winterberg  ^  demon- 
strated this  latter  effect  clearly,  and  showed  that  in  a  heart  under  the 
influence  of  atropin  fibrillation  ceases  coincidently  with  the  cessation  of 
faradic  stimulation,  whereas  in  a  heart  without  atropin  fibrillation  per- 
sists as  an  after-effect.  It  is  therefore  suggested  that  depression  of 
auricular  conductivity  is  an  important  factor  in  the  production  of  auri- 
cular fibrillation.      Digitalis  and  strophanthus  have  the  same  effect 

1  Lewis,  T.,  "Galvanometric  Curves  yielded  by  Cardiac  Beats  Generated  in 
Various  Areas  of  the  Auricular  Musculature.  The  Pacemaker  of  the  Heart,"  Heart, 
Lond.,  1910-11,  ii.,  23. 

^  Einthoven,  W.,  "  Weiteres  iiber  das  Elektrokardiogramm,"  Arch.  f.  d.  ges. 
Physiol.,  Bonn,  1908,  cxxii.,  517. 

3  Gaskell,  W.  H.,  "  On  the  Innervation  of  the  Heart,  with  Especial  Reference 
to  the  Heart  of  the  Tortoise,"  Journ.  of  Physiol.,  Camb.,  188.3,  iv.,  43. 

*  Mac  William,  J.  A.,  "  On  the  Phenomena  of  Inhibition  in  the  Mammalian 
Heart,"  ibid.,  1888,  ix.,  345. 

s  Winterberg,  H.,  "  Ueber  Herzilimmern  und  seine  Beeinflussung  durch  Kampher," 
Zeitschr.f.  exp.  Pathol,  u.  Therap.,  Berlin,  1906,  iii.,  182  ;  "  Studien  liber  Herzflimmern," 
Arch.f.  de  ges.  Physiol.,  Bonn,  1907,  cxvii.,  223  ;  1908,  cxxii.,  361. 


iM..\'ri<:  w'l 


pi  — 


THE   ACTION   OF  THE   VAGUS  101 

as  vagus  stimulation  in  promoting  the  onset  of  auricular  fibrillation, 
for,  as  will  be  shown  later,  these  drugs  tend  to  transform  auricular 
flutter  into  fibrillation.  Erom  the  preceding  argument  it  is  evident 
that  they  do  so,  probably  by  blocking  the  transmission  of  stimuli  in  the 
auricular  walls. 

Y.  Tonicity. — From  Gaskell's  ^  classical  experiments  we  know  that 
the  tone  of  the  heart  muscle  in  the  tortoise,  frog,  and  toad  is  lowered 
by  stimulation  of  the  vagus  and  raised  by  stimulation  of  the  augmentor 
nerve.  Meek  and  Eyster^  demonstrated  a  similar  slow  positive  varia- 
tion of  potential  in  the  heart  of  the  tortoise  under  vagus  stimulation, 
and  some  of  my  own  records  from  the  human  subject  show  it  likewise 
(Fig.  89).  The  change  probably  indicates  depression  of  tone  in  the 
heart  muscle  under  vagus  stm-iulation. 

2.  Effects  on  the  Atrio-venteicular  Conducting  System 

From  the  work  of  Gaskell,^  Mac  William,^  Muskens*  and  other 
physiologists  it  is  well  known  that  in  the  animal  heart  the  con- 
duction of  stimuli  to  the  ventricles  may  be  impaired  by  means  of  vagus 
stimulation.  When  the  human  heart  is  beating  with  a  physiological 
rhythm  vagus  compression  seldom  depresses  the  conductivity  of  the 
atrio-ventricular  bundle  unless  there  be  some  antecedent  impairment 
of  its  function.  An  exceptional  instance  of  vagus  compression  causing 
partial  block  in  a  healthy  heart  is  shown  in  Fig.  88.  In  many  cases 
of  auricular  flutter,  however,  compression  of  one  or  other  vagus  induces 
well-marked  blocking  of  stimuli  to  the  ventricles  (see  p.  104). 

As  yet  we  have  little  reliable  information  regarding  the  influence 
of  vagus  stimulation  and  paralysis  on  the  excitability  of  the  branches 
of  the  bundle.  If  those  extrasystoles  that  are  termed  "ventricular" 
arise  in  the  branches  of  the  bundle,  as  seems  probable,  the  onset  or 
abolition  of  such  extrasystoles  by  means  of  vagus  stimulation  or 
paralysis  might  yield  information  of  interest  and  value.  But  our 
knowledge  of  this  matter  is  still  imperfect.  One  fact  that  we  do  know 
is  that  in  cases  of  heart  failure  extrasystoles  may  disappear  under  the 

1  Gaskell,  W.  H.,  "  On  the  Innervation  of  tlie  Heart,  with  Especial  Eeference  to 
the  Heart  of  the  Tortoise,"  Journ.  of  Physiol,  Camb.,  1883,  iv.,  43. 

-  Meek,  W.  J.,  and  Eyster,  J.  A.  E.,  "Electrical  Changes  in  the  Heart  during 
Vagus  Stimulation,^'  Amer.  Journ.  of  Physiol.,  Boston,  1912,  xxx.,  271. 

3  MacWilliam,  J.  A.,  "  On  the  Phenomena  of  Inhibition  in  the  ]\Ianimalian  Heart," 
ibid.,  1888,  ix.,  345. 

•*Muskens,  L.  J.  J.,  "An  Analysis  of  the  Action  of  the  Vagus  Xerve  on  the 
Heart,"  Amer.  Journ.  of  Physiol.,  Boston,  1898,  i.,  486. 


102     THE  ACTION   OF  THE   VAGUS   AND   SYMPATHETIC 

influence  of  digitalis,  one  action  of  which  is  to  stimulate  the  vagus. 
This  restoration  of  a  wholly  normal  rhythm,  however,  may  be  clue  to 
other  factors  than  mere  depression  of  excitability  in  the  branches  of 
the  atrio-ventricular  bundle.  Moreover,  the  frequency  of  ventricular 
extrasystoles  is  seldom  or  never  lessened  by  compression  of  the  vagus, 
and  in  some  instances  their  frequency  is  apparently  lessened  while  the 
heart  is  under  the  influence  of  atropin. 


3.  Effects  on  the  Ventkicles 

The  vagi  have  but  little  direct  influence  on  the  ventricles.  This  is 
proved  by  the  fact  that  in  cases  of  complete  heart-block  the  rate, 
rhythm,  and  strength  of  the  ventricular  beats  are  uninfluenced  either 
by  vagus  stimulation  or  paralysis. 

"When  the  ventricles  are  responding  in  a  physiological  manner  to  each 

7'rtstu.Tt  OTi  of/ 


Ex 


Fig.  90. — After  compression  of  the  right  vagus  there  is  one  extrasystole  (Ex),  which  is  followed 
by  transient  alternation  of  the  pnlse. 

supra-ventricular  stimulus,  however,  the  vagus  acts  upon  the  ventricles 
indirectly  through  the  auricles,  and  the  former  seldom  fail  to  follow 
the  rate  and  rhythm  set  by  the  latter.  In  such  instances  vagus 
stimulation  may  occasionally  depress  the  contractility  of  the  ventricles, 
for  the  initial  ventricular  beats,  after  pronounced  vagus  inhibition,  may 
only  gradually  attain  their  full  strength.  Under  these  circumstances 
a  pulse  tracing  presents  an  ascending  staircase. 


4.  Aftee-effects  of  Vagus  Stimulation 

The  inhibitory  effects  on  the  auricles  usually  pass  off  gradually, 
successive  beats  becoming  quicker  and  stronger.  In  the  atrio- 
ventricular conducting  system  the  rate  of  recovery  may  be  either 
slower  or  faster  than  in  the  auricles.  The  escape  of  the  ventricles  from 
vagus  inhibition  may  be  synchronous  with  that  of  the  auricles,  but  in 
many-  instances  the  auricles  are  the  first  to  escape. 

The  only  other  after-effect  to  which  reference  need  be  made  is  the 


THE   ACTIOX   OF  THE   VAGUS   IN   ELUTTEll         103 

occasional  onset  of  extrasystoles  during  the  period  of  escape  from  vagus 
inhibition.  They  are  probably  due  to  sympathetic  stimulation — for 
this  is  known  to  promote  their  onset.  Moreover,  the  vagus  contains 
sympathetic  fibres,  and  the  latent  period  of  sympathetic  stimulation  is 
longer  than  that  of  inhibition  (Fig.  90). 

II.  The  Action  of  the  Sympathetic  ox  the  Nokmal  Heart 

The  sympathetic  influences  the  heart  in  a  manner  the  reverse  of 
the  vagus.  The  most  striking  effects  of  sympathetic  stimulation  are 
acceleration  of  rate,  shortening  of  systole,  and  stronger  contraction  of 
auricles  and  ventricles.  The  conduction  of  stimuli  to  the  ventricles  is 
also  improved.  In  electrocardiograms  the  height  of  the  deflexions 
P  and  T  is  increased,  whereas  that  of  B  is  reduced.  The  quickened 
and  forcible  action  of  the  heart  under  the  intiueuce  of  emotional 
disturbance  and  of  substances  such  as  adrenalin,  and  the  action  of  the 
heart  in  exophthalmic  goitre,  are  examples  of  sympathetic  stimulation. 

In  other  instances  the  physiological  rhythm  of  the  heart  may  be 
disturbed,  for  when  the  left  accelerator  is  stimulated,  according  to 
Eothberger  and  Winterberg,^  the  left  auricle  may  begin  to  contract 
before  the  right.  This  change  is  expressed  by  inversion  of  the  auri- 
cular deflexion  P.  The  same  observers  have  shown  that  extrasystoles 
are  liable  to  occur  when  the  vagus  and  sympathetic  are  stimulated 
simultaneously. 

III.  The  Action  of  the  Vagus  in  Aueicular  Flutter 

1.  The  Action  on  the  Auricles. — It  has  already  been  mentioned  that 
physiological  beats  of  the  auricles  are  under  vagus  control.  They  are 
retarded  and  weakened  by  vagus  stimulation.  In  contrast  thereto, 
it  is  found  that  in  all  cases  of  flutter  in  which  compression  of  either 
vagus  was  recorded  this  failed  to  influence  the  auricles.  Their  rate  and 
the  form  of  their  electrocardiographic  deflexions  remained  unchanged. 
It  has  therefore  been  suggested  by  Cohu  ^  that  flutter  may  be  due  either 
to  the  inhibitory  influences  of  the  vagus  failing  to  reach  the  sinus  node, 
or  to  failure  on  the  part  of  the  node  to  respond  to  the  vagus,  and  that 

1  Rotliberger,  J.,  and  Winterberg,  H.,  "  Ueber  die  Bezieliuiigen  der  Herznerven  zur 
Form  des  Elektrokardiogranims,"  Arch.  f.  d.  ges.  Physiol,  Bonn.,  1910,  cxxxv.,  506. 

2  Cohii,  A.  E.,  "  Auricular  Tachycardia,  witli  a  Consideration  of  Certain  Differ- 
ences between  the  Two  Vagi,"  Journ.  of  Kxjier.  Med.,  Xew  York,  1912,  xv.,  49. 


104     THE   ACTION   OF   THE   VAGUS   AND   SYMPATHETIC 

in  either  case  the  dominant  site  of  stimulus  production  is  elsewhere 
than  in  the  sinus  node.  The  latter  hypothesis  is  in  harmony  with 
MacWilliam's  classical  experiments  on  the  production  of  flutter  by 
faradic  stimulation  of  the  auricular  appendix,  and  with  the  abnormal 
form  of  the  auricular  deflexion  P,  in  nearly  every  recorded  case  of 
auricular  flutter. 

Digital  compression  of  the  vagus  is  a  mild  form  of  vagus  stimu- 
lation. If  stronger  stimulation  be  applied,  as  in  experimental  work 
when  the  exposed  vagus  is  faradised,  this  does  not  retard  the  flutter  or 
cause  the  auricular  beats  to  revert  directly  to  a  physiological  rhythm, 
but  induces  either  auricular  fibrillation  or  a  form  of  auricular  action 
in  which  flutter  and  fibrillation  are  combined  as  described  on  p.  26. 
According  to  Eobinson,^  the  normal  rhythm  may  sometimes  be  restored 
several  seconds  after  the  cessation  of  vagus  stimulation. 

2.  The  Action  on  the  Atrio-mntricidar  Concluding  System  and  the 
Ventricles. — In  most  cases  of  auricular  flutter  in  which  the  effects  of 
vagus  compression  were  recorded  the  ventricular  rate  was  retarded 
although  the  auricles  continued  in  flutter.  This  effect  was  not 
observed  in  Case  I.,  but  here  there  was  complete  heart-block.  In 
Cases  IV.,  VL,  and  L.,  likewise,  compression  of  the  vagus  did  not  retard 
the  ventricles,  but  the  efl'ect  was  seen  in  Cases  II.,  III.,  V.,  XV.,  XVI., 
XVII.,  XXIV.,  XXV.,  and  XXVI.  The  ventricular  slowing  is  illus- 
trated in  Plates  XIII.  and  XVIII.  In  both  instances  the  escape  from 
vagus  inhibition  is  gradual. 

In  attempting  to  ascertain  how  the  ventricular  retardation  is 
induced,  we  have  to  remember  that  it  is  similar  to  that  obtained  by 
MacWilliam  ^  upon  stimulation  of  the  inhibitory  area  of  the  mammalian 
auricles  (see  p.  25).  The  retardation  is  not  due  to  any  lessening  of  the 
rate  of  the  auricles  nor,  so  far  as  can  be  determined,  to  any  weakening 
of  their  beats.  Moreover,  it  is  almost  certainly  not  due  to  any  depres- 
sion of  ventricular  excitability,  for  we  know  that  vagus  stimulation  has 
little,  if  any,  influence  on  this  function  of  the  ventricular  muscle. 
Again,  the  effect  cannot  be  ascribed  to  depression  of  contractility  in 
the  ventricles,  for  there  is  no  ascending  staircase  during  the  period 
of  escape  from  vagus  inhibition ;  on  the  contrary,  the  arterial  pulse 
waves  are  of  large  amplitude  (Plate  XIIL).    We  are  therefore  driven  to 

1  Robinson,  G.  Canby,  "  The  Influence  of  the  Vagus  Nerves  on  the  Faradized 
Auricles  in  the  Dog's  Heart,"  Journ.  of  Eoyer.  Med.,  New  York,  1913,  xvii.,  429. 

2  MacWilliam,  J.  A.,  "  On  the  Phenomena  of  Inhibition  in  the  Mammalian  Heart," 
Journ.  of  Physiol..,  Camb.,  1888,  ix.,  345-. 


LATh:    w 


THE   SYMrATHETIC   IX   FLUTTEK  105 

the  conclusion  that  the  ventricular  retardation  obtained  by  compression 
of  either  vagus  in  cases  of  auricular  flutter  is  due  to  depression  of 
conductivity  in  the  atrio-ventricular  Itundle  whereby  fewer  stimuli — 
for  example,  1  in  10  instead  of  1  in  2  or  1  in  4 — are  transmitted  to  the 
ventricles. 

IV.  The  Action  of  the  Sympathetic  in  Auricular  Flutter 

Eegarding  this  matter  our  knowledge  is  still  imperfect.  In  some 
cases  paroxysmal  attacks  of  flutter  are  apparently  brought  on  by 
emotional  disturbance,  excitement,  or  worry.  In  Case  XXIII.,  for 
example,  the  patient,  a  clergyman,  attributed  many  of  his  attacks  to 
excitement,  and  found  that  they  often  followed  his  Sunday  evening's 
sermon.  But  although  in  some  cases  sympathetic  stimulation  has  a 
definite  etiological  relation  to  the  onset  of  flutter,  the  sympathetic 
seems  to  have  little,  if  any,  influence  on  the  auricles  after  flutter  has 
been  established.  In  each  individual  case  the  rate  of  the  fluttering 
auricles  usually  remains  remarkably  constant,  and  is  very  slightly,  if 
at  all,  affected  by  any  form  of  psychical  stimulation. 


CHAPTER  VIII 
THE  ACTION  OF  DEUGS  OF  THE  DIGITALIS  GROUP 

I.  Digitalis 

Digitalis  has  been  administered  in  about  50  per  cent,  of  the  recorded 
cases.  When  the  auricles  are  in  flutter  the  drug  exerts  a  profound 
influence  on  the  heart,  and  the  effects  are  similar  to  those  of  vagus 
stimulation. 

At  first  the  drug  does  not  check  the  flutter,  but  lowers  the  rate  of 
the  ventricles  and  often  renders  their  rhythm  irregular.  The  ventricles, 
which  had  previously  been  responding  to  every  alternate  auricular  beat, 
may  now  respond  to  every  third  auricular  beat  so  that  the  ventricular 
rate  falls,  for  example,  from  150  to  100  per  minute,  and  the  rhythm 
remains  regular.  In  other  instances  the  first  recorded  change  is  that 
the  ventricles  respond  to  a  varying  number  of  auricular  beats.  The 
rhythm  of  the  ventricles  then  becomes  irregular  and  their  rate  is 
somewhat  lessened.  This  phase  may  be  of  short  duration  and  is 
therefore  liable  to  pass  unnoticed  or,  because  of  the  ventricular 
irregularity,  to  be  mistaken  for  auricular  fibrillation. 

During  the  second  phase  the  ventricles  respond  rhythmically  to 
every  fourth  auricular  beat,  and  consequently  the  ventricular  rate  falls 
to  about  70-80  per  minute.  As  a  rule  the  patient  now  obtains  much 
relief  from  all  his  distressing  symptoms. 

The  third  phase  begins  when  the  rapid  rhythmic  co-ordinate  beats 
of  the  auricles  become  replaced  by  inco-ordinate  fibrillar  contractions. 
The  rate  of  the  ventricles  is  not  necessarily  much  accelerated,  and  is 
indeed  often  under  80  per  minute,  but  their  rhythm  becomes  wholly 
irregular.  In  some  instances  the  ventricular  beats  are  coupled,  and 
the  pause  after  the  second  beat  of  each  couple  is  then  inconstant.  In 
electrocardiograms  the  first  beat  of  each  couple  is  shown  to  be  a 
response  to  a  supra-ventricular  stimulus,  whereas  the  second  beat  has 
the  character  of  a  ventricular  extrasystole.  The  second  beat  of  each 
couple  may  fail  to  open  the  aortic  valve,  and  the  rate  of  the  arterial 
pulse  is  then  one-half  of  the  true  ventricular  rate. 

When  the  auricles  pass  into  fibrillation  no  new  symptoms  arise. 


DIGITALIS   AND   STIiOPHAXTHUS  107 

On  the  contrary,  the  improvement  in  the  patient's  condition  is  usually 
maintained,  and  he  may  even  feel  remarkably  well  and  he  able  to  walk 
about  without  discomfort. 

The  fourth  phase  is  characterised  by  restoration  of  the  physiological 
rhythm.  In  some  instances  this  may  occur  while  the  patient  is  still 
taking  digitalis,  but  as  a  rule  not  until  the  drug  has  been  discontinued. 
The  restoration  of  normal  rhythm  has  been  observed  as  early  as  the 
third  or  as  late  as  the  twenty-third  day  after  the  patient  has  ceased 
taking  digitalis.  How  long  the  physiological  rhythm  may  be  main- 
tained we  do  not  know,  but  in  Case  XIX.  it  was  apparently  maintained 
for  at  least  three  years.  In  other  instances,  however,  tlie  physiological 
rhythm  is  not  maintained  permanently,  but  is  interrupted  from  time 
to  time  by  paroxysms  of  flutter  (Cases  XA'III.,  XXIII.),  flutter  and 
fibrillation  (Cases  VI.,  XXXIV.),  or  occasional  supra- ventricular 
ex trasy stoles  (Case  XXXIII.).  Extrasy stoles  have  also  been  recorded 
Ijy  Korteweg  ^  as  an  after-effect  of  experimental  auricular  flutter  in 
the  cat. 

All  four  phases  are  not  constantly  observed  in  every  case  of  auricular 
flutter  treated  with  digitalis.  The  first  phase  may  be  brief  and  pass 
unnoticed.  The  second  phase  is  seldom  omitted.  The  third  phase — 
that  of  auricular  fibrillation — may  not  develop  for  several  reasons. 
The  digitalis  may  not  have  been  given  in  sufficient  doses.  In  Case  II. 
the  patient  took  1-455  minims  in  the  course  of  thirty-one  days  before 
the  auricles  passed  into  fibrillation.  In  Case  XXIII.  485  minims 
were  given  in  the  course  of  nine  days  before  fibrillation  ensued.  In 
other  instances  (Case  XXIV.,  for  example),  the  onset  of  nausea, 
vomiting,  and  diarrhoea  may  necessitate  the  drug  being  withdrawn 
before  fibrillation  is  induced.  Yet  even  in  such  cases  the  patient's 
symptoms  may  be  relieved  by  the  fall  in  the  ventricular  rate.  Lastly, 
the  physiological  rhythm  may  never  be  restored  fully,  either  because 
auricular  fibrillation  persists  in  spite  of  digitalis  having  been  with- 
drawn, or  because  the  degree  of  heart  failure  is  so  profound  that  the 
administration  of  the  drug  has  to  be  continued. 

11.    STROPHA^'THUS 

The  action  of  strophanthus  is  essentially  the  same  as  that  of 
digitalis.  In  Case  III.,  with  auricular  flutter  at  a  rate  of  320  per 
minute,  an   intravenous   injection   of   strophanthin   induced   auricular 

1  Korteweg,  A.  J.,  Arhythmie  door  Atrium-fihrillatie,  Proefsclirift,  Leideu,  191-3. 


108      THE   ACTION  OF  DEUGS  OF   THE   DIGITALIS   GEOUP 

fibrillation,  and  lowered  the  ventricular  rate  from  160  to  96-104  per 
minute.  On  the  following  day  the  heart  regained  its  physiological 
rhythm.  In  Cases  XXIY.  and  XXV.  strophanthus  produced  the  same 
effects  as  had  previously  been  obtained  with  digitalis. 

III.  Sqltill 

Under  the  administration  of  squill,  as  recorded  by  Hay,^  a  ratio  of 
As  :  Ys  : :  3  : 1  changed  to  4:1.  Three  weeks  later  the  auricles  were  in 
fibrillation,  and  subsequently  the  normal  rhythm  was  restored.  In 
Case  I.  the  auricular  flutter  was  not  converted  into  fibrillation  by 
digitalis,  strophanthus,  or  squill. 

In  auricular  flutter  the  results  obtained  by  the  drugs  of  the  digitalis 
group  are  similar  to  those  of  vagus  stimulation.  The  initial  effect  of 
digitalis — retardation  of  ventricular  rate  alone — is  identical  with  that 
of  vagus  compression.  The  subsequent  conversion  of  auricular  flutter 
into  fibrillation,  when  the  administration  of  digitalis  is  continued,  is 
similar  to  the  effect  obtained  experimentally  on  the  fluttering  auricles 
by  faradisation  of  the  vagus.  There  is  consequently  good  reason  for 
concluding  that  in  auricular  flutter  digitalis  acts  by  vagus  stimulation, 
and  that  the  primary  effect  of  the  drug  is  to  depress  the  conductivity 
of  the  atrio-ventrieular  bundle,  thus  blocking  the  transmission  of 
stimuli  to  the  ventricles.  This  conclusion  is  strengthened  by  the  fact 
that  atropin  may  induce  a  transient  abolition  of  the  ventricular 
retardation,  as  recorded  by  Eihl  (Case  XV.),  and  Hume  (Case  XXX). 

The  essential  similarity  of  action  between  vagus  stimulation  and 
digitalis  leads  us  to  the  further  conclusion  that  when  the  drug  induces 
fibrillation,  it  does  so  by  depressing  conductivity  within  the  auricular 
walls. 

As  we  know  that  auricular  flutter  may  be  a  phase  of  auricular  activity 
intermediate  between  a  physiological  rhythm  and  fibrillation,  the  question 
arises  whether  there  is  a  similar  phase  of  flutter  after  fibrillation  ceases 
and  before  the  normal  rhythm  is  restored,  or  whether  the  auricles 
revert  directly  from  fibrillation  to  a  normal  rhythm.  Certain  clinical 
and  experimental  observations  lend  support  to  the  latter  hypothesis. 
According  to  Korteweg,-  when  fibrillation  following  experimental 
"  auricular   tachycardia "   ceases,    the   action   reverts   to  a   slow,  weak 

^  Hay,  J.,  "  Two  Gases  of  Auricular  Flutter,"  Lancet,  Lond.,  1913,  ii.,  986. 

2  Korteweg,  A.  J.,  Arhythmie  door  Atrium-fibrillatie,  Proefschrift,  Leiden,  1913. 


UESTORATION   OF   NOPtMAL   EllYTHM 


109 


=;  B 


co-ordinate  contraction.  Again,  Lewis  ^ 
points  out  that  a  rhythniic  tachycardia 
induced  by,  and  persisting  after,  stimula- 
tion of  some  portion  of  the  heart  may  be 
abolished  wlien  a  still  faster  rate  of  con- 
traction, subsequently  induced,  has  sub- 
sided. Moreover,  it  has  been  suggested 
by  Cushny-  that  the  period  of  slower 
contractions  with  pauses  succeeding  arti- 
ficial acceleration  of  the  isolated  ven- 
tricles is  due  to  depression  of  the 
function  of  stimulus  production  in  the 
ventricular  pacemaker,  namely,  to  its 
fatigue.  Similarly,  when  the  physiologi- 
cal beats  of  the  auricles  have  been 
replaced  by  fibrillation,  and  the  latter 
in  turn  has  ceased,  a  pause  ensues  before 
the  physiological  beats  begin  again.  This 
pause  must  be  regarded  as  indicating 
either  fatigue,  or  inhibition  of  the 
physiological  pacemaker  by  the  fibrilla- 
tion. When  auricular  fibrillation  suc- 
ceeds flutter,  the  sites  wherein  both  the 
fluttering  and  the  physiological  beats 
were  initiated  might  be  supposed  to 
suffer  fatigue,  and  if  the  former  site 
were  the  more  fatigued  the  latter  might 
be  the  first  to  recover  its  function  after 
fibrillation  ceases.  Under  such  circum- 
stances the  normal  rhythm  of  the  heart 
would  be  restored. 

Although  in  some  instances  there 
may  be  a  direct  change  from  fibrilla- 
tion, following  flutter,  to  a  normal 
rhythm,    this     sequence    has     not     yet 

^  Lewis,  T.,  "  Observations  upon  a  Curious 
and  not  uncommon  Form  of  Extreme  Accelera- 
tion of  the  Auricle.  '  Auricular  Flutter,' "  Reart, 
Loud.,  1912-13,  iv.,  171. 

2  Cushny,  A.  R.,  "Stimulation  of  the  Isolated  Ventricle,  with  Special  Reference  to 
the  Development  of  Spontaneous  Rhythm,"  Head,  Limd.,  1911-12,  iii.,  257. 


-€ 


110     THE   ACTION   OF  DRUGS   OF   THE   DIGITALIS   GEOUP 

been  recorded  clinically.  It  is  not  improbable  that  in  some  instances 
there  may  be  an  intermediate  phase  of  flutter,  so  brief  that  it  has 
uniformly  escaped  recognition  in  the  human  heart.  In  the  cat's  heart 
this  brief  phase  has  been  recorded  by  W.  E.  Hume,  who  has  kindly 
permitted  me  to  make  use  of  the  record  in  Fig.  92.  While  the  auricles 
were  in  flutter  under  the  influence  of  weak  faradic  stimulation  applied 
to  the  left  auricle,  the  left  vagus  was  faradised  and  fibrillation  ensued. 
When  the  vagus  stimulation  was  discontinued,  the  fibrillation  became 
replaced  by  flutter;  when  the  faradisation  of  the  auricle  ceased  the 
flutter  terminated,  and  after  a  short  pause  the  normal  rhythm  was 
re-established. 


CHAPTER  IX 

DIAGNOSIS 

Whenever  a  patient  complains  of  sudden  attacks  of  palpitation  and 
dyspnoea,  with  or  without  precordial  pain,  syncope,  or  other  symptoms, 
and  the  pulse-rate  during  the  attack  attains  or  exceeds  130  or  140  per 
minute,  auricular  flutter  should  be  suspected.  If  the  pulse  during  the 
attack  is  absolutely  rhythmic,  the  condition  is  probably  due  to  flutter. 
Moreover,  if  the  attack  of  rhythmic  tachycardia  comes  on  suddenly, 
and  either  ends  abruptly  or  the  rate  of  the  rhythmic  pulse-beats  falls  to 
one-half,  while  the  patient  is  taking  digitalis,  the  auricles  are  almost 
certainly  in  flutter.  In  many  instances  paroxysmal  or  persistent 
attacks  of  auricular  flutter  have  probably  been  misinterpreted  as  auricular 
fibrillation,  or  have  been  designated  by  the  vague  term  "  paroxysmal 
tachycardia."  Errors  in  diagnosis  are  especially  liable  to  arise  when  the 
ventricular  rhythm  is  irregular,  because  auricular  fibrillation  is  then 
closely  simulated.  In  such  cases  a  correct  diagnosis  can  seldom  be  made 
without  the  aid  of  the  polygraph.  Even  this  may  fail  to  differentiate 
between  flutter  and  fibrillation,  and  the  true  action  of  the  auricles  may 
not  be  revealed  until  electrocardiograms  have  been  obtained. 

The  conditions  for  which  auricular  flutter  is  liable  to  be  mistaken 
are :  1.  Physiological  rhythm  without  acceleration ;  2,  physiological 
rhythm  with  acceleration ;  3,  extrasystolic  arrhythmia ;  4,  nodal 
1  hvthm ;    and  5,  auricular  fibrillation. 


I.  Physiological  PtHYTHM  without  Acceleration 

When  the  auricles  are  fluttering,  and  the  ventricular  rate  is  con- 
stantly one-third  or  one-fourth  of  the  auricular  rate,  the  cardiac 
impulse  and  the  arterial  pulse  are  rhythmic  and  their  rate  is  not 
notably  accelerated.  In  Case  XXX.,  for  example,  the  ventricular  rate 
was  usually  about  87  per  minute.  In  Case  II.,  the  rate  was  68-72 
for  sixteen  days  while  the  patient  was  taking  digitalis;  and  in  Case 
XII.,  with  partial  heart-block,  the  ventricular  rate  w\as  42  when  the 
auricular   rate   was    200   per   minute.      It   is    therefore   evident   that 


112  DIAGNOSIS 

auricular  flutter  may  readily  be  overlooked  when  the  patient  is  taking 
digitalis  or  when  there  is  partial  heart-block.  Under  these  circum- 
stances it  may  be  impossible  to  determine,  without  the  aid  of  instru- 
mental records,  whether  the  rhythm  is  physiological  or  whether  the 
auricles  are  in  flutter. 

Two  observations  may  be  helpful.  Firstly,  the  patient  should  be 
directed  to  breathe  deeply.  When  the  auricles  are  in  flutter  the  rate 
of  the  ventricles  does  not  hurry  with  inspiration  and  slow  with  expira- 
tion, as  often  occurs,  in  more  or  less  marked  degree,  when  the  cardiac 
rhythm  is  physiological.  Secondly,  the  patient  should  be  asked  to  make 
some  comparatively  slight  physical  effort,  such  as  is  entailed  by  sitting 
up  in  bed  or  walking  across  the  room.  In  a  heart  with  a  normal 
rhythm  this  effort,  though  usually  causing  some  acceleration,  does  not 
cause  sudden  doubling  of  the  ventricular  rate,  say  from  80  to  160  per 
minute,  whereas  this  instability  and  tendency  to  sudden  doubling  of 
the  ventricular  rate  are  not  infrequent  in  auricular  flutter. 

Polygraph  records  are  usually  of  much  assistance  in  diagnosis.  In 
a  case  of  auricular  flutter  with  a  ratio  of  As  :  Vs : :  3  :  1,  the  series  of 
three  auricular  waves  for  each  beat  of  the  arterial  pulse  may,  however, 
be  regarded  erroneously  as  the  a,  c,  and  v  waves  of  a  physiological 
rhythm.  This  fallacy  has  been  discussed  by  Hume,^  who  showed  that 
in  the  case  of  flutter  which  he  recorded  the  third  wave  was  not  a  pure 
V  wave  because  its  summit  was  attained  after  the  opening  of  the 
tricuspid  valve.  In  this  group  of  cases  the  first  of  the  three  waves 
is  a  pure  a  wave ;  the  second  is  composed  of  a  and  c,  and  in  contrast 
with  a  pure  c  wave  has  usually  a  more  or  less  rounded  summit ;  the 
third  wave  represents  a  and  v  waves  fused  in  one. 

Again,  when  the  rate  of  the  ventricles  is  constantly  one-fourth  of 
the  auricular  rate,  a  physiological  rhythm  may  be  simulated.  In  Case 
II.,  for  example,  the  cardiac  impulse  and  arterial  pulse  were  rhythmic, 
at  a  rate  of  68-72  for  sixteen  days,  although  the  auricles  were  mean- 
while in  flutter  at  a  rate  of  268-276  per  minute.  The  four  waves  c-\-a, 
a,  a,  and  a  in  the  jugular  tracing  (Fig.  78)  might  be  mistaken  for  c,  v,  h, 
and  a  waves  of  a  normal  rhythm.  In  a  normal  rhythm,  however,  the 
summits  of  the  four  waves  are  not  uniformly  equidistant  from  one 
another.  For  example,  in  Fig.  7  the  interval  between  c  and  h  is 
constant,  whereas  that  between  h  and  a,  or  h  and  the  succeeding  c,  is 
inconstant.     Moreover,  the   rounded   summit   of   the  compound  wave 

1  Hume,  W.  E.,  "  A  Case  in  which  a  High  Speed  of  the  Auricles  did  not  produce 
Tachycardia,"  Quart.  Journ.  of  Med.,  Oxford,  1912-13,  vi.,  235. 


SINUS   TACHYCAIJDIA 


113 


c  +  a  ill  auiicular  Hiitter  dilTers  from  the  sliai[»-iiointc(]  sumniit  of  the 
wave  f  in  a  noiiiial  ilivtlini. 


II.    PllYSlOLOiilCAL    lillVTHM    WITH    AUCELEIIATKJN    (SiNUS    TA<'IlVrAUDIA) 

This  is  the  most  frequent  form  of  tachycardia.  It  may  Ije  due  to 
})hysiological  causes  such  as  physical  exertion  and  emotion  influencing  a 
perfectly  healthy  heart,  or  to  pathological  causes.  As  examples  of  the 
latter,  mention  may  be  made  of  the  various  acute  exanthemata,  lobar 
pneumonia,  pulmonary  tuberculosis,  exophthalmic  goitre,  acute  endo- 
carditis and  myocarditis,  and  chronic  valvular  disease  with  cardiac 
dilatation  and  dropsy. 

When  the  heart,  in  spite  of  acceleration,  maintains  its  physiological 
rhvthm,  the  onset  and  termination  of  the  tachvcardia  are  both  suradual, 


Fig.  03. — Sinu.s  tachycardia,  at  the  rate  of  97  per  minute,  and  puLsus  alternans  in  a  man,  aged  57,  with 
lieart  failure.    .Jugulo-carotid  and  brachial  tracings.    Tlie  o-c  interval  i.s  0"24  second. 

and  the  rate  seldom  exceeds  140  per  minute,  even  although  there  be 
marked  myocardial  enfeeblement.  Thus  in  fifteen  cases  of  exophthalmic 
goitre  I  found  maximum  rates  of  83,  90,  97,  100.  107,  110, 114, 115,  117, 
122,  128,  129,  131,  147  and  148  per  mimite.  In  none  of  these  cases 
was  the  As  — Vs  interval  less  than  0-13  second,  or  more  than  0*17 
second;  it  was  usually  0'14  second — the  normal  interval.  Again,  in 
sub-acute  endocarditis  with  a  physiological  rhythm  the  rate  seldom 
rises  to  150  or  160  per  minute,  but  I  have  seen  cases  in  which  the  latter 
rate  was  attained.  Moreover,  I  have  seldom  observed  the  ventricular 
rate  to  exceed  135  per  minute  in  cases  of  chronic  valvular  disease  so 
long  as  the  physiological  rhythm  was  maintained. 

Polygraph  records  and  electrocardiograms  are  of  aid  in  diagnosis. 
"When  the  heart's  rhythm  is  physiological  and  the  rate  greatly  acceler- 
ated, each  carotid  impulse  in  a  jugular  tracing  is  preceded  by  only  one 
auricular  wave.  Owing  to  the  curtailment  of  ventricular  diastole  each 
auricular  wave  is  partially,  or  wholly,  fused  with  the  c  wave  of  the 

8 


114 


DIAGIS^OSIS 


antecedent  ventricular  beat  (Fig.  93).  In  an  electrocardiogram  there 
is  likewise  one  deflexion  P  for  each  group  of  ventricular  deflexions,  and 
P  is  superposed  on  the  antecedent  T  deflexion  because  of  the  shortened 
ventriculo-diastolic  phase  (Fig.  95).  The  As  — A"s  interval,  as  repre- 
sented by  the  P —  ()  interval,  is  seldom  less  than  0-14  second — the 
normal  interval — even  when  the  heart's  rate  is  120  or  130  per  minute. 

The  superposition  of  a  upon  v,  and  of  P  upon  T,  implies  that  the 
auricles  begin  to  contract  before  the  antecedent  ventricular  systole  has 
terminated.  As  the  auricles  contract  at  a  time  when  the  auriculo- 
A^entricular  valves  are  closed  they  cannot  drive  onwards  the  blood  they 
contain.  It  therefore  follows  that  any  pre-existing  mitral  presystolic 
murmur  disappears,  and  that  each  auricular  systole  probably  causes  a 
retrograde  wave  in  the  great  veins,  as  shown  by  the  large  wave  r  +  a  in 


1 

t\    s: 

\ 

V 

"\ 

\ 

^ 

■\ 

U    ^ 

1 

1 

u    ^ 

\ 

V 

\ 

\ 

x 

\ 

\ 

Fig.  9i. — Diagrams  to  show  that  when  the  auricles  are  in  rhythmic  flutter  irregularity  of  the  ventricular 
responses  may  simulate  (f.)  an  auricular  extrasystole  "siith  a  pause  that  is  not  fully  compensatory,  or 
(6)  a  ventricular  estrasystole  with  a  fully  compensatory  pause. 

the  jugular  tracings.  It  is  thus  evident  that  when  the  ventricular  rate 
is  greatly  accelerated  marked  pulsation  of  the  jugular  veins  and  dis- 
appearance of  a  mitral  presystolic  murmur  do  not  necessarily  indicate 
loss  of  the  physiological  rhythm. 


III.    EXTEASYSTOLIC    AeEHYTH.MIA 

Auricular  flutter  is  most  liable  to  be  mistaken  for  extrasystolic 
arrhythmia  when  the  patient  is  taking  digitalis,  yet  before  a  ratio  of 
As  :  Ys  : :  4  : 1  is  fully  developed.  A  supra-ventricular  extrasystole. 
with  a  pause  that  is  not  fully  compensatory,  is  simulated  when  a  con- 
stant ratio  of  4:1  is  momentarily  interrupted  by  a  ratio  of  2:1,  as  in 
Fig.  94,  a.  In  Case  II.  the  auriculo-ventricular  ratio  was,  at  one  time, 
frequently  changing  from  4 :  1  to  2:1,  and  the  regular  coupling  of  the 
cardiac  impulse  and  arterial  pulse  used  to  suggest  a  regularly  recurring 
supra-ventricular   extrasystole  (Fig.  97).      A  ventricular   extrasystole 


I'LA'll';    MX. 


.1  ( 


Q  Q 


/^  w^  wA,  y^  w/Av^  ^^ 


liliillliliiliiiiiiiuiiiiiiiiitiiiiiiniiiiiiiniiiiiiiiiiiiiiiiiiiuiiiiliuiiiiii 


Fill.  '.1'). — Sinus  tachycardia  at  a  rate  of  131  per  minute  in  a  case  of  aortic  and 
mitral  incompetence.     Derivation  III.    1  cm.  =  1  millivolt. 


Fig.  9G. — Eacli  physiological  beat  is  followed  by  two  extrasystoles,  in  the  second  of  which  the  auricular 
deflexion^^P  is  inverted.    Male,  aged  49.    Derivation  II. 


VMS 


Fig.  97. — Aiuicular  flutter  at  a  rate  of  2S1  per  minute.  The  ventricle.s  usually  respond  to  every 
second  auricular  beat,  but  occasionally  to  everj'  fourth.  Case  II.  (IStli  August  1012).  Derivation 
II.     1  eni.  =  l  millivolt. 


EXTIIASYSTOLTC   AllKHYTHIMIA  115 

would  be  simulated  if  tlie  auriculo-veiitriculai'  ratio  clianged  moment- 
arily from  3:1  to  2  :  1,  4: 1,  and  then  back  to  3  :  1  (Fig.  94,  Z>).  In 
cases  of  this  nature  polygrapli  tracings  or  electrocardiograms  will 
establish  the  diagnosis. 

Auricular  flutter  may  be  simulated  still  more  closely  by  a  paroxysmal 
attack  in  which  each  beat  is  a  ventricular  extrasystole.  This  is  a 
somewhat  rare  form  of  paroxysmal  tachycardia.  In  Fig.  96,  from  a 
man  aged  49,  extrasystoles  occur  in  pairs  after  eacli  physiological 
beat.  In  the  second  beat  of  each  pair  the  auricular  deflexion  is  in- 
verted, and  there  is  a  long  post-extrasystolic  pause  before  the  next 
pliysiological  beat.  In  another  case,  that  of  a  man  aged  39  who  was 
suffering  from  aortic  and  mitral  incompetence,  the  ventricular  extra- 
systoles  were  sometimes  "  single,"  and  at  other  times  there  were  series 
of  two,  three,  four,  live,  or  more  extrasystoles  in  rapid  succession,  only 


Fifi.  OS. ^Paroxysmal  tacliycardia  due  to  ventricular  extrasystoles  in  a  case  of  aortic  and  mitral  incompetence. 
Brachial  and  apical  tracings.  The  last  nine  beats  of  a  long  paroxysm  are  shown.  After  the  post-extrasystolic 
pause,  which  is  fully  compensatory,  there  are  two  normal  beats  and  thereafter  another  paroxysm  begins. 

the  last  beat  of  each  series  being  followed  by  a  post-extrasystolic  pause. 
Fig.  98,  from  this  case,  shows  the  end  of  a  long  paroxysm  of  extra- 
systoles at  a  rate  of  153  per  minute.  This  paroxysm  is  succeeded  by 
a  fully  compensatory  post-extrasystolic  pause.  Two  normal  beats  then 
occur,  and  thereafter  another  paroxysm  of  extrasystoles  begins.  In  the 
case  described  by  Stuart  Hart  ^  there  were  similar  paroxysms,  lasting 
from  a  few  seconds  to  three  minutes,  in  which  ventricular  extrasystoles 
recurred  rhythmically  at  a  rate  of  240  per  minute.  Hoffmann  ^  has  also 
recorded  a  case  of  this  nature. 

IV.  Nodal  Ehythm 

A  nodal  extrasystole,  as  defined  on  p.  15,  is  a  premature  and 
synchronous  beat  of  the  aviricles  and  ventricles.  A  nodal  rhythm  is 
a  series  of  rhythmic  or  arrhythmic  beats  in  which  the  auricles  and 
ventricles  contract  simultaneously.     Each  ventricular  beat  may  start 

1  Hart,  T.  Stuart,  "Paroxysmal  Tachycardia,"  Heart,  Lond.,  1912-13,  iv.,  128. 

2  Hoffmann,  A.,  Die  Elektrographie,  Wiesbaden,  1914,  Case  xix.,  250-252. 


116  DIAGNOSIS 

before  the  auricles  begin  to  contract ;  the  auricles  and  ventricles  may 
begin  to  contract  at  the  same  moment;  or  each  auricular  contraction 
may  precede  that  of  the  ventricles,  but  in  this  case  the  As  -  Vs 
interval  is  much  shorter  than  normal. 

The  site  of  origin  of  the  dominant  stimuli  in  nodal  rhythm  has 
been  the  subject  of  much  discussion.  It  is  not  in  the  ventricles,  because 
electrocardiograms  demonstrate  that  these  chambers  are  contracting  in 
response  to  supra-ventricular  stimuli.  Moreover,  the  site  of  stimulus 
production  is  presumably  not  in  the  general  auricular  musculature, 
the  sinus  node,  or  the  wall  of  the  coronary  sinus,  because  if  the 
stimuli  did  arise  in  these  situations  it  would  have  to  pass  through  the 
atrio-ventricular  node  before  reaching  the  ventricles,  and  it  is  in  this 
node,  according  to  Hering,-  that  the  transmission  of  supra-ventricular 
stimuli  suffers  delay.  The  synchronism  of  auricles  and  ventricles  in 
nodal  extrasy stoles  and  nodal  rhythm  suggests  that  the  stimuli  for 
contraction  are  generated  at  a  site  approximately  midway  between 
these  chambers,  and  presumably  in  the  atrio-ventricular  node  or  bundle. 
According  to  this  hypothesis  nodal  rhythm  results  from  the  acquire- 
ment by  these  structures  of  the  power  of  initiating  stimuli  for  con- 
traction at  a  greater  rate  than  the  sinus  node.  The  functional  activity 
of  the  atrio-ventricular  node  or  bundle  has  become  unduly  exalted,  or 
that  of  the  sinus  node  has  become  depressed,  or  both  changes  have 
occurred  simultaneously. 

Nodal  rhythm  was  described  by  Lohmann  ^  as  resulting  from  stimu- 
lation of  the  septum  in  the  region  of  the  node  and  bundle  ;  by  Lohmann  ^ 
and  Hering,'^  as  a  result  of  destructive  lesions  at  the  cavo-auricular 
junction;  by  Eihl^  and  Hering^  as  an  effect  of  accelerator  stimulation; 
and  by  Cushny,^  after  injection  of  dogs  with  aconitine.     The  site  of 

1  Lohmann,  A.,  "  Zur  Automatie  der  Briickenfasern  und  der  Ventrikel  des 
Herzens,"  Arch.  f.  Anat.  u.  Physiol.  (Physiol.  Abt.),  Leipz.,  1904,  431. 

2  Hering,  H.  E.,  "  Nachweis,  dass  die  Verzogerung  der  Erregungsiiberleitung 
zwischen  Vorhof  und  Kammer  des  Saugethierherzens  im  Tawara'schen  Knoten 
erfolgt,"  Arch.f.  d.  ges.  Phtjsiol.,  Bonn,  1910,  cxxxi.,  572. 

3  Lohmann,  A.,  "  Ueber  die  Funktion  der  Briickenfasern  an  Stelle  der  grossen 
Venen  die  Fiihrung  der  Herztatigkeit  zu  iibernehmen,"  ibid.,  1908,  cxxiii.,  628. 

^Hering,  H.  E.,  " Experimentelle  Studien  an  Saugethieren  iiber  das  Elektro- 
kardiogramni,"  ibid..,  1909,  cxxvii.,  155. 

^  Rihl,  J.,  "Experimentelle  Analyse  des  Venenpulses  bei  den  durch  Extra- 
systolen  verursachten  Unregelmassigkeiten  des  Saugethierherzens,"  Zeitschr.  f.  exp. 
Pathol  u.  Thercq}.,  Berlin,  1905,  i.,  43. 

^  Hering,  H.  E.,  "Einiges  iiber  die  Ursprungsreize  des  Saugetierherzens  und  ihre 
Beziehung  zum  Accelerans,"  Zentralb.f.  Physiol.,  Leipz.,  1905,  xix.,  129. 

■^  Cushny,  A.  R.,  "  The  Irregularities  of  the  Mammalian  Heart  observed  under 
Aconitine  and  on  Electrical  Stimulation,"  Heart,  London,  1909-10,  i.,  1. 


NODAL   EHYTHM  117 

origin  of  the  stininli  has  hctMi  (hscussed  in  a  critical  paper  hy  Erlanger.^ 
Among  the  most  instructive  experimental  observations  are  those  of 
Eothberger  and  "Winterberg.-  These  observers  found  that  in  almost 
every  instance  the  accelerator  fibres  passing  to  the  cavo-auricular 
junction  could  be  put  out  of  action  by  the  local  application  of  ethyl 
chloride  spray,  and  that  subsequent  stimulation  of  the  left  accelerator 
uniformly  induced  a  nodal  rhythm  with  synchronous  contractions  of 
the  auricles  and  ventricles.  While  the  nodal  rhythm  was  developing, 
the  auricular  detiexions  became  gradually  merged  in  those  of  the  ven- 
tricles until  eventually,  when  the  auricles  and  ventricles  were  beating 
synchronously,  the  auricular  detiexions  were  no  longer  visible.  The 
jugular  pulsations  were  then  of  strikingly  large  amplitude.  This 
phenomenon  may  also  be  observed  in  cases  of  nodal  rhythm  in  man 
(see  Fig.  99). 

The  most  notable  cases  of  nodal  rhythm  in  the  human  heart  are 
those  described  by  Cowan  ^  and  by  Hoffmann.'^  In  Cowan's  cases  the 
cardiac  rhythm  was  regular,  and  the  rate  varied,  being  sometimes  very 
frequent  (over  200  per  minute),  but  in  other  instances  only  slightly 
accelerated.  The  nodal  rhythm  was  either  intermittent  and  paroxysmal, 
or  persistent.  In  all  the  cases  recorded  by  Cowan  the  a-c  interval  in 
the  jugular  tracings  was  notably  shorter  than  normal.  Cowan,  Fleming, 
and  Kennedy,^  have  described  inflammatory  changes  in  the  atrio- 
ventricular node  of  six  cases  of  acute  endocarditis  with  persistent  nodal 
rhythm.  This  rhythm  has  also  been  described  by  Rihl  ^  and  Lewis ; " 
it  has  been  observed  in  cases  of  rheumatism,  typhoid  fever,  and 
scarlatina   by   Belski,  ^  and    in   cases   of   diphtheria    by    Hecht  "^   and 

1  Eiianger,  J.,  "  The  Localization  of  Imimlse  Initiation  and  Conduction  in  the 
Heart,"  Arcli.  of  Intern.  Med.,  Chicago,  1913,  xi.,  .3.34. 

-  Rothberger,  C.  J.,  and  Winterberg,  H.,  "  Ueber  die  Beziehungen  der  Herznerven 
zur  atrio-ventrikulaien  Aiitomatie  (nodal  rhythm),"  Arch.  f.  d.  ges.  Physiol,  Bonn, 
1910,  cxxxv.,  559. 

3  Cowan,  J.,  Diieases  of  the  Heart,  Lond.,  1914,  1.33-158. 

■*  Hoffmann,  A.,  "  Die  Elektrographie  als  Untersuchungsmethode  des  Herzens 
und  ihre  Ergebnisse,"  Wiesbaden,  1914,  202-247. 

°  Cowan,  J.,  Fleming,  G.  B.,  and  Kennedy,  A.  M.,  Trans.  XYIIth  Internat. 
Conr/ress  of  Med.,  London,  1914,  Sect.  YI.  Med.,  Part  IL,  223. 

•^  Rihl,  .J.,  "  Ueber  atrioventrikuliire  Tachycardie  beim  Menschen,"  Deidsch.  med. 
Wochenschr.,  1907,  xxxiii.,  632. 

'  Lewis,  T.,  "Auricular  Fibrillation  and  its  Relationship  to  Clinical  Irregularity 
of  the  Heart,"  Heart,  Lond.,  1909-10,  i.,  306. 

'^  Belski,  A.,  "  Beobachtungen  liber  atrioventrikuliire  Automatie  im  Yerlauf  der 
Infektionskrankheiten,"  Zeit.schr.  f.  klin.  Med.,  Berlin,  1909,  Ixvii.,  515. 

^  Hecht,  A.  F.,  "  Ueber  atrioventrikuliire  Automatie  bei  post-diphtherischer 
Herzschwiiche,"  Wien.  med.  Wochenschr.,  1912,  Ixii.,  2015. 


118 


DIAGNOSIS 


Hume.^     IsToclal  rhythm   may  be  the   precursor   of,  or   may  alternate 
with,  either  auricular  flutter  or  fibrillation. 

The  Venous  Pulse. — In  clinical  work  the  differentiation  of  auricular 
flutter  from  nodal  rhythm  is  not  yet  possible  without  the  aid  of  poly- 
graph tracings  or  electrocardiograms.  In  the  former,  the  apical  impulse 
begins  before  or  simultaneously  with  the  auricular  wave  in  the  jugular 


Fig.  99. — Nodal  rhythm  beginning  abruptly  and  passing  off  gradually.  In  the  first  three  beats  and  in  the  last 
beat  the  contraction  of  the  auricles  (1)  precedes  that  of  the  ventricles  (2) ;  whereas  in  the  nodal  beats  the 
ventricles  begin  to  contract  before  the  auricles,  and  the  auricular  wave,  a,  in  the  jugular  vein  is  of  large  size. 
While  the  nodal  rhythm  is  passing  off,  the  interval  2-1  becomes  progressively  shorter  until,  eventually,  the 
contraction  of  the  auricles  again  precedes  that  of  the  ventricles. 


tracings,  or  the  interval  between  the  contraction  of  auricle  and  ventricle 
is  notably  short.  In  consequence  of  the  auricles  being  in  contraction 
at  the  same  time  as  the  ventricles,  the  former  cannot  expel  their  blood 
into  the  latter,  and  the  auricular  wave  in  the  jugular  veins  is  therefore 
of  large  size.  The  onset  of  nodal  rhythm  is  well  shown  in  Fig.  99, 
obtained   from  a  joiner   aged  47,  who  was   suffering   from   sub-acute 

1  Hume,  W.  E.,  "A  Polygraphic Study  of  Four   Cases  of  Diphtheria,   with  a 
Pathological  Examination  of  Three  Cases,"  Heart,  London,  1913-14,  v.,  25. 


XODAL  IIHYTHM  119 

myocarditis  witli  cyanosis,  dyspnoea,  and  other  signs  of  heart  failure. 
When  the  patient  first  came  under  observation  the  pulse-rate  was 
usually  about  70  per  minute;  the  rhythm  was  normal  and  the  venous 
tracing  presented  distinct  a,  c,  and  v  waves,  as  in  the  first  three  beats  of 
Fig.  99.  In  the  next  five  beats  of  Fig.  99,  however,  the  rhythm  is  not 
normal,  because  the  ventricles  begin  to  contract  before  the  auricles.  In 
the  apical  tracing  the  auricular  wave  is  no  longer  visible,  whereas  in  the 
venous  tracing  it  is  of  large  size.  In  the  first  and  second  beats  of  the 
nodal  rhythrii  (the  4th  and  5th  beats  recorded  in  Fig.  99),  the  Ys  — As 
interval  is  0-20  and  0-25  second  respectively.  Thereafter  theVs  — As 
interval  becomes  gradually  shorter  with  each  successive  beat,  until 
eventually  the  auricular  contraction  again  precedes  that  of  the  ventricles. 
This  gradual  transition  from  a  nodal  to  a  normal  rhythm  is  similar  to 
that  recorded  by  Rothberger  and  "Winterberg.^ 

For  a  month  after  the  record  in  Fig.  99  was  obtained  the  heart's 
rhythm  varied  from  normal  to  nodal.  With  a  normal  rhythm  the  rate 
was  about  90,  with  a  nodal  rhythm  about  79  per  minute.  The  patient's 
general  condition  improved  greatly,  and  he  resumed  his  work.  About 
one  month  later,  however,  he  again  became  cyanosed,  very  breathless 
and  dropsical.  The  auricles  were  then  found  to  be  in  fibrillation. 
Cheyne-Stokes  breathing  developed,  the  dropsy  became  progressively 
worse,  and  the  patient  gradually  sank  and  died  three  and  a  half  months 
after  he  first  came  under  my  observation. 

At  the  post-mortem  examination  all  the  chambers  of  the  heart  were 
found  to  be  dilated ;  the  left  ventricle  was  hypertrophied  and  presented 
abundant  patches  of  fibrosis.  The  valves  were  all  healthy.  The  lungs 
showed  chronic  venous  congestion  and  hypostatic  pneumonia.  On 
microscopic  examination,  the  walls  of  all  the  chambers  of  the  heart 
revealed  widespread  fibrosis  and  pronounced  cellular  infiltration.  In 
the  auricular  septum  there  was  much  engorgement  of  the  small  vessels, 
and  many  haemorrhages.  The  atrio-ventricular  node  and  bundle  were 
markedly  involved  by  the  inflammatory  infiltration,  but  the  branches 
of  the  bundle  were  implicated  to  a  lesser  degree. 

Electrocafdiograras. — The  ventricular  deflexions  in  nodal  rhythm  are 
essentially  of  normal  character,  indicating  supra- ventricular  stimulation. 
The  auricular  deflexion  is  either  (1)  synchronous  with,  and  masked  by 
the  ventricular  deflexions,  or  (2)  precedes  the  initial  ventricular  deflexion 

1  Rothberger,  C.  .J.,  and  Winterberg,  H.,  "  Ueber  die  Beziehungen  der  Herznerven 
zur  atiio-ventrikulareii  Automatie  (nodal  rhythm),"  Arch.  f.  d.  ges.  Physiol.,  Bonn, 
1910,  cxxxv.,  559. 


120  DIAGNOSIS 

by  an  interval  that  is  decidedly  shorter  than  normal,  and  is  of  atypical 
form. 

The  first  variety  of  nodal  rhythm  is  illustrated  in  Fig.  100,  obtained 
from  a  woman,  aged  49,  affected  with  mitral  incompetence.  For  two 
years  she  had  been  suffering  from  dyspnoea  and  palpitation,  and  she  had 
been  dropsical.  While  she  was  in  hospital  her  auricles  were  usually  in 
fibrillation.  On  one  occasion,  however,  all  the  beats  were  probably 
responses  to  stimuli  arising  in  the  atrio -ventricular  conducting  system, 
and  as  in  the  cases  described  by  Eppinger  and  Stoerk,i  Mathewson^  and 
others,  the  form  of  the  ventricular  deflexions  indicates  that  the  stimuli 
were  reaching  the  ventricles  through  one  or  other  branch  of  the  bundle, 
but  not  through  both  branches  simultaneously.  The  stimuli  for  the 
beats  lettered  X  in  Fig.  100  probably  originated  in  the  right  and  left 
branch  of  the  bundle,  but  in  neither  instance  did  the  stimulus  pass  back 
to  the  auricles.  In  each  of  the  remaining  beats,  how^ever,  the  stimulus 
passed  not  merely  forwards  to  the  ventricles  but  also  backwards  to  the 
auricles,  as  shown  by  the  deflexion  P. 

The  second  variety  of  nodal  rhythm  is  represented  in  Fig.  101.  The 
patient  was  a  Crimean  veteran,  aged  72,  under  the  care  of  Professor 
Kussell  in  the  Royal  Infirmary.  For  about  six  months  the  patient  had 
been  suffering  from  headache,  dyspnoea,  dropsy,  and  other  symptoms  of 
heart  failure.  Soon  after  his  admission  to  hospital,  orthopnoea  became 
very  intense,  and  the  legs  became  swollen  up  like  bolsters.  The  apex- 
beat  was  in  the  normal  situation,  but  was  unduly  forcible.  No  murmurs 
were  audible.  The  arteries  of  the  arms  were  thick,  and  the  systolic 
pressure  was  200  mm.  Hg.  The  cardiac  rhythm  was  almost  constantly 
irregular  owing  to  numerous  auricular  extrasystoles,  each  of  which 
yielded  an  inverted  P  deflexion  and  a  short  P  —  R  interval  (0"10 
second),  whereas  the  corresponding  interval  of  the  normal  beats  was 
0"14  second. 

On  several  occasions  when  the  heart  was  grossly  irregular,  each  beat 
was  initiated  by  an  auricular  contraction  yielding  an  abnormal,  inverted 
deflexion  of  the  same  form  as  that  of  the  isolated  auricular  extrasystoles 
(Fig.  101).  On  these  occasions  the  irregularity  of  the  pulse  was  so 
pronounced  as  to  simulate  auricular  fibrillation  very  closely.  Under 
the  influence  of  rest,  digitalis,  and  squill,  the  patient  made  a  satisfactory 

1  Eppinger,  H.,  and  Stoerk,  O.,  "Zur  Klinik  des  Elektrokardiogramnis,"  Zeitschr. 
f.  Min.  Med.,  Berlin,  1910,  Ixxi.,  157. 

2  Matliewson,  G.  D.,  "  Lesions  of  the  Branches  of  the  Auriculo-ventricular  Bundle," 
Heart,  Lend.,  1912-13,  iv.,  385. 


TLATF.    XX. 


Fig.  100.-  X(xlal  anliytlimia  with  two  extrasystole.s  (X).    From  a  woman,  aged  41),  witli  mitral  incompetence. 
Derivation  II.     1 -.5  cm.  =1  millivolt. 


iiuiiiiiiiiiiiiiiiiiiiitiiHiiiiiiniininiiitiiiiiiiiiiiiiuiiuiaiiiuuiiitiiiiiiiiumiiuuiuiiiuiiiiiiiimiuiiiiJiiij 

Fig.  101.— Xodal  rhvthm.    The  heart'.s  action,  at  a  rate  of  95  per  minute,  is  wholly  irregular.    The  ventricles  respond 
to  auricular  beats  which  are  represented  by  the  atypical  deflections  P.    Derivation  II.     1--5  cm.  =  l  millivolt. 


IlllllillllllilllllllllllllllllllllllllllllllllllllllllllllllllilllliiiilllllllllllllllllllllllllllllllllllilllllllllllllllllllllllillU 
Fig.  102.— Auricular  fibrillation  with  a  ventricular  rate  of  100  per  minute.     Derivation  II.     1  cm.  =  l  millivolt. 


NODAL    IIIIYTII.AI  121 

recovery  ;  he  lost  all  his  dyspncea  and  dropsy ;  his  heart  regained  its 
normal  rhythm  except  for  an  occasional  extrasystole;  and  in  tiie  course 
of  a  few  months,  when  he  was  able  to  return  home,  he  was  in  enjoyment 
of  better  health  then  that  of  many  a  man  of  his  years. 

In  this  case  there  was  a  heterotopic  site  of  stimulus  production 
giving  rise,  at  first,  to  isolated  supra-ventricular  extrasystoles  and 
subsequently  to  a  series  of  beats  similar  in  character  and  irregular  in 
rhythm.  The  exact  site  of  stimulation  cannot  be  defined,  for  although, 
according  to  Lewis,^  inverted  auricular  deflexions  represent  nodal 
stimulation  this  hypothesis  is  not  established,  and  according  to 
liothberger  and  Winterberg-  the  auricular  defiexion  is  of  this  form 
when  the  left,  instead  of  the  right,  auricle  initiates  the  contraction. 

Eliythmic  " imroxysmal  tachycardia"  is  probably  more  often  auricular 
flutter  than  nodal  rhythm.  In  some  of  the  cases  recorded  by  Hoffmann  ^ 
the  sudden  doubling,  or  halving,  of  the  ventricular  rate,  and  the  ven- 
tricular retardation  effected  by  compression  of  the  vagus,  suggest  the 
possibility  of  auricular  flutter.  But  the  following  was  probably  an 
example  of  paroxysmal  nodal  rhythm. 

The  patient  was  a  woman,  aged  33,  without  any  history  of  rheumatism, 
who  had  suffered  for  eight  years  from  occasional  attacks  of  "  flying  of 
the  heart."  As  a  rule  each  attack  was  preceded  by  nausea  and  sickness, 
lasted  for  about  one  day,  and  passed  off  gradually.  When  she  was 
admitted  to  the  Eoyal  Infirmary  under  the  care  of  Dr.  Chalmers  Watson, 
"  her  heart  had  been  flying  for  a  week."  During  the  first  month  of  her 
residence  in  hospital  a  number  of  paroxysms  were  observed. 

"When  the  cardiac  rhythm  was  normal,  the  rate  was  about  80-90 
per  minute,  the  arterial  pulse  was  of  good  volume,  and  the  jugular 
pulse  was  small.  The  heart  was  not  enlarged  and  no  murmurs  were 
audible. 

During  the  attacks,  which  lasted  for  a  few  hours  to  several  days,  the 
ventricles  were  beating  rhythmically  at  a  rate  of  168-226  per  minute ; 
the  pulse  in  the  arteries  of  the  arm  became  almost  imperceptible 
whereas  the  pulsations  of  the  jugular  veins  became  so  forcible  as  to 
resemble  violent  throbbing  of  the  carotid  arteries.      The  liver  could 

^  Lewis,  T.,  "Auricular  Fibrillation  and  its  Relationship  to  Clinical  Irregulaiity 
of  the  Heart,"  Heart,  Lond.,  1909-10,  i.,  .306. 

-  Rothhergev,  C.  J.,  and  "Winterberg,  H.  "  Ueber  die  Beziehungen  der  Herznerveu 
zur  atrio-ventrikuliiren  Automatie  (nodal  rhythm),''"  Arch.  f.  d.  fjes.  Pluj.nol.,  Bonn, 
1910,  cxxxv.,  559. 

3  Hort'inann,  A.,  "Xeue  Beobachtungen  iiber  Herzjagen,"  Deutsch.  Arch.  f.  klin. 
Med.,  Leipz.,  1903,  Ixxviii.,  39. 


122  DIAGNOSIS 

be  felt  to  pulsate  freely,  the  heart  sounds  acquired  the  fcetal  rhythm, 
and  if  the  attack  was  a  prolonged  one  the  patient  became  very 
breathless. 

On  two  occasions  an  attack  came  on  suddenly  while  the  armlet  of 
the  polygraph  was  being  adjusted.  The  ventricular  rate  rose  abruptly 
from  90  to  195,  and  from  84  to  222,  per  minute.      Fifteen  minutes  after 


[Fig.  103. — Paroxysmal  tachycardia  witli  a  rate  of  224  per  minute.    Jugulo-carotid  and  brachial  pulsations. 

the  second  of  these  attacks  had  began,  the  patient  was  questioned 
regarding  her  symptoms,  and  was  found  to  be  wholly  unaware  of  the 
attack.  On  one  occasion  when  the  effect  of  change  of  posture  was 
tested,  the  pulse-rate  was  found  to  rise  from  168  to  226  per  minute 
when  the  patient  sat  up  in  bed  (Fig.  103).  Compression  of  neither 
vagus  slowed  the  pulse. 

V.   AUEICULAE   FlBPJLLATIOX 

Both  in  its  paroxysmal  and  in  its  persistent  forms,  auricular 
flutter  may  be  mistaken  for  fibrillation.  As  a  rule  the  perfectly 
rhythmic  action  of  the  ventricles  excludes  the  possibility  of  auricular 
fibrillation.  But  difficulty  may  arise  when  the  ventricular  rate  is  very 
fast  or  when  the  ventricular  rhythm,  in  flutter,  is  irregular. 

When  auricular  flbrillation  is  combined  with  a  very  rapid  action  of 
the  ventricles  —  for  example,  160-180  per  minute  —  the  irregularity 
is  often  so  slight  that  it  may  be  unrecognisable  on  palpation  of  the 
pulse  and  apex-beat  or  on  auscultation  of  the  heart-sounds. 

Fig.  102  was  obtained  from  a  case  of  this  nature.  The  patient  was 
a  tall,  thin  man,  aged  61,  who  showed  no  trace  of  cyanosis  or  oedema. 
He  had  been  short  of  breath  for  six  weeks.  The  apex-beat  was 
forcible  but  in  normal  position ;  the  flrst  sound  at  the  apex  was 
impure,  the  second  sound  was  clear  and  accentuated.  The  arteries 
were  moderately  thickened,  and  the  urine  was  albuminous.  The 
ventricular  rate  was  159  per  minute.  Definite  auricular  deflexions, 
■  of  small  amplitude  and  irregular  rhythm,  characteristic  of  auricular 
fibrillation,  were  not  visible  except  during  an  occasional  long  ventricular 


AURICULAR   FIBRILLATION  123 

diastole.  As  a  rule  the  auricular  dellexions  were  inconspicuous ;  never- 
theless auricular  fihrillaliun  was  indicated  by  the  slight  irrregularity  of 
the  ventricles,  and  by  the  varying  form  of  the  curve  between  S  and  B 
in  successive  cycles.  In  cases  of  this  nature,  a  little  irregularity  of 
the  pulse  suggesting  auricular  fibrillation  can  usually  be  recognised 
even  by  the  finger  alone. 

Auricular  fibrillation  is  simulated  still  more  closely  when  the 
ventricles  are  responding  irregularly  to  fluttering  auricles ;  for  example, 
when  successive  ventricular  contractions  are  in  response  to  4,  3,  and  2 
auricular  beats.  This  in  itself  renders  the  ventricular  rhythm  irregular, 
and  the  irregularity  is  intensified  further  by  the  fact  the  As  - Vs  interval 
is  longer  when  the  ratio  of  As  :  Ys  is  3 : 1  than  when  it  is  4 : 1  (Fig.  82). 
Under  these  circumstances,  digital  examination  of  the  pulse,  palpation 
of  the  apex-beat,  and  auscultation  of  the  heart-sounds  may  fail  to 
differentiate  between  flutter  and  fibrillation.  In  such  cases  compression 
of  the  right  vagus  may  be  helpful.  In  my  experience  this  usually 
retards  the  ventricles  when  the  auricles  are  in  flutter,  and  frequently 
fails  to  do  so  when  the  auricles  are  in  fibrillation.  A  pronounced 
ventricular  retardation  upon  compression  of  one  or  other  vagus 
consequently  suggests  flutter  rather  than  fibrillation. 

It  sometimes  happens  that  a  greatly  accelerated  and  markedly 
irregular  action  of.  the  ventricles  suddenly  becomes  absolutely  rhythmic 
while  the  rate  remains  very  fast,  say  150  per  minute.  This  change  may 
occur  frequently  within  the  course  of  a  few  minutes.  It  indicates 
either  that  auricular  fibrillation  and  flutter  are  alternating  with  each 
other,  or  that  with  persistent  flutter  the  ventricular  responses  are  some- 
times irregular  (for  example,  3:1,  2:1,  4:1,  3:1)  and  sometimes 
regular  (for  example,  2:1,  2:1,  2:1). 

Simple  sphygmographic  tracings  may  suffice  to  demonstrate  that 
the  arterial  pulse-beats  are  wholly  arrhythmic,  indicating  fibrillation, 
or  that  groups  of  beats  are  of  identical  duration,  indicating  a  rhythmic 
auricular  action  (Figs.  75  and  104).  In  auricular  fibrillation  the  height 
of  the  pulse-wave  in  a  sphygmographic  tracing  bears  no  constant  rela- 
tion to  the  length  of  the  preceding  pulse  period.  This  has  been  regarded 
as  a  definite  indication  of  auricular  fibrillation.  The  same  inconstant 
relation,  however,  is  often  observed  when  the  auricles  are  fluttering 
and  the  ventricles  responding  to  a  varying  number  of  auricular  beats 
(Fig.  104). 

If  polygraph  tracings  reveal  a  rhythmic  series  of  large  auricular 
waves  in  the  jugular  veins  at  times  when  the  ventricles  are  in  diastole. 


124 


DIAGNOSIS 


the 


the  condition  is  clearly  flutter  and  not  fibrillation. 
Even  although  the  auricular  waves  in  the  jugular 
pulse  are  not  large,  the  auricles  are  almost  cer- 
I  tainly  in  flutter  if  the  arterial  pulse-beats  occur 
=  in  groups  of  equal  length,  as  in  Fig.  104.  On  the 
^  other  hand,  if  the  auricular  waves  are  small, 
^  irregular  in  rhythm  and  very  rapid,  and  if  at  the 
"i     same  time  there   is   little  or  no  uniformity  in  the 

1  grouping  of  the  arterial  pulse-beats,  the  auricles 
=.  are  either  in  fibrillation  or  in  the  form  of  activity 
^'     represented    by    simultaneous   flutter   and   fibrilla- 

2  tion.  Again,  if  the  jugular  pulse  is  of  the  ven- 
=  tricular  form  and  the  rhythm  of  the  ventricles  is 
g  wholly  irregular  the  auricles  are  in  fibrillation, 
H  whereas  a  jugular  pulse  of  the  same  form  associ- 
I  ated  with  a  rapid  and  rhythmic  action  of  the 
i  ventricles  almost  certainly  indicates  auricular 
I    flutter. 

S  Electrocardiograms    afford    the     most     reliable 

.=  means  of  diagnosis,  but  unfortunately  they  are 
P  not  always  available.  In  almost  every  recorded 
I  case  of  flutter  the  auricular  deflexions  are  of 
I  constant  form,  rhythmic,  large  and  comparatively 
7  infrequent  at  a  rate  of  about  200-370  per 
J  minute.  In  fibrillation  the  auricular  deflexions 
I  are  irregular  in  form  and  rhythm,  of  small  ampli- 
X  tude  and  greater  rate  (380-520  or  more  per 
I  minute).  The  distinctive  features  are  usually  seen 
5     best    in    records    taken    by    derivation    III.    (left 

hand  and  left  foot),  and  with  a  comparatively 
slack  flbre.  If  the  auricular  deflexions  are  ob- 
scured as  a  result  of  excessive  ventricular  acceler- 
ation, their  true  form  may  often  be  revealed  by 
means  of  compression  of  the  right  vagus  in  the 
neck  (Plate  XIII.,  Eig.  65). 

The   most   difficult    cases   of    all   are   those   in 
which  the  auricular  action  is  frequently  changing 
from   flutter    to    fibrillation,    and    those   in   which 
auricular    action    is    a    combination    of   flutter  and    fibrillation   as 


PLATE  XXI. 


f  I 


AUEICULAR   riBEILLATION 


125 


described  on  pages  26,  93,  ami  94.     The  clinical  features  in  the  latter 
cases  resemble  ainicular  lil)iillution  more  closely  than  llutter. 


Flo.  107. — Auricular  lUittrr  Avith  uiarUiHi  irro^ularity  of  tlui  arterial  pulse.     Case  VI.     Jugulo-carotid 

and  brachial  tJaciiiK's. 


Lastly,  it  should  be  remembered  that  flutter  is  often  the  percursor 
of  persistent  fibrillation,  and  that  many  cases  presenting  the  latter  form 
of  auricular  action  have  probably  passed  through  an  unrecognised 
phase  of  flutter. 


CHAPTER   X 

PROGNOSIS 

As  only  a  limited  number  of  cases  have  hitherto  been  recorded,  and  as 
most  of  them  were  under  observation  for  only  a  short  period  of  time, 
the  statistical  evidence  on  which  to  base  a  prognosis  is  necessarily 
scanty.  Certain  general  conclusions,  however,  may  be  drawn  from 
a  survey  of  the  recorded  cases. 

In  one  group  of  cases  the  normal  cardiac  rhythm  is  eventually 
restored,  and  either  the  patient  makes  an  apparently  complete  recovery 
and  remains  well  for  several  years,  or,  failing  that,  his  general  condi- 
tion is  greatly  improved.  The  normal  rhythm  was  restored  in  twenty- 
two  out  of  fifty-three  cases.  One  patient  (Case  IV.)  was  perfectly  well 
five  months  after  a  sharp  attack  of  flutter.  In  Case  XIX.,  the  patient 
was  seriously  ill  when  the  auricles  were  fluttering,  yet  the  heart 
regained  its  physiological  rhythm  ;  three  years  later  the  patient  was 
in  o-ood  health,  and  had  no  trouble  with  his  heart.  In  Case  XXXII. 
auricular  flutter  passed  into  fibrillation,  but  four  and  a  half  years 
later  the  normal  cardiac  rhythm  was  found  to  be  restored  and  the 
patient  was  earning  his  living.  In  Case  VIIL,  the  patient  was  in 
excellent  health  four  years  after  a  prolonged  attack  of  tachycardia 
almost  certainly  due  to  flutter. 

A  second  group,  a  large  one,  comprises  the  cases  with  paroxysmal 
attacks  of  flutter  recurring  from  time  to  time  over  a  period  of  several 
years.  In  Case  XXXIX.  attacks  recurred  occasionally  during  a  period 
of  two  years.  In  Case  XVIII.  they  recurred  at  intervals  during  at 
least  eleven  yea,rs.  In  Cases  XXIII.  and  XXIV.,  in  which  auricular 
flutter  was  subsequently  demonstrated,  there  had  been  a  liability  to 
paroxysmal  attacks  of  tachycardia  for  thirty  and  thirty-eight  years 
respectively. 

A  third  group  consists  of  cases  in  which  auricular  flutter  persists 
more  or  less  continuously  for  many  weeks,  months,  or  even  years. 
Flutter  persisted  for  four  months  in  Case  XIII.,  for  six  months  in  Case 
XXV.,  for  nine  months  in  Case  XIV.,  for  eighteen  months  in  Case  XVI., 
and  for  nearly  five  years  in  Case  I.     Even  after  the  flutter  has  persisted 


PROGNOSIS  127 

for  years,  however,  the  auricles  may  eventually  regain    their   normal 
rhythm  (see  Case  I.). 

A  fourth  group,  one  of  considerable  magnitude,  includes  eases  in 
which  flutter  is  the  iprecursor  of  a  more  or  less  persistent  auricular 
fibrillation.     This  sequence  was  observed  in  Cases  II.,  V.,  and  XLVII. 

A  fifth  group  is  constituted  by  cases  in  which  a  fatal  issue  ensued. 
In  Cases  III.  and  XXXVI.  death  occurred  ten  and  nineteen  days 
respectively  after  the  first  records  of  fiutter  had  been  obtained.  In 
Case  XII.  seven  weeks  elapsed  between  the  onset  of  flutter  and  the 
patients  tleath.  In  Case  XXI.  the  patient  died  nineteen  months  after 
the  onset  of  his  illness.  In  Case  XXIII.  there  had  been  paroxysmal 
attacks  of  tachycardia  for  thirty  years  before  death.  When  the  fatal 
issue  supervenes  it  may  be  sudden,  as  in  Cases  VI.,  XII.,  XXI.,  and 
LIIL,  or  gradual  as  in  Cases  XI.,  XXXV.,  and  XXXVII. 

The  prognosis  is  more  favourable  when  the  heart  and  vessels  are 
apparently  healthy  than  when  there  is  obvious  disease  of  the  myocardium 
or  valves,  or  definite  arterio-sclerosis. 

Again,  an  initial  attack  of  fiutter  will  probably  be  milder  and 
shorter  than  subsequent  attacks.  Indeed,  the  recovery  from  a  first 
attack  is  probably  invariably  complete  for  a  time  at  any  rate,  unless 
there  be  advanced  disease  of  the  myocardium,  as  in  acute  infective 
myocarditis  or  in  the  terminal  phases  of  mitral  disease. 

During  an  attack  of  flutter  the  severity  of  the  dyspnoea,  the  intensity 
of  the  cyanosis,  and  the  urgency  of  other  symptoms  furnish  the  best 
guide  to  prognosis.  Alternation  of  the  pulse  when  the  rate  is  only 
120  per  minute  is  usually  an  unfavourable  sign  ;  but  wiien  the  rate  is 
150  or  more,  alternation  is  not  necessarily  serious.  Its  absence  when 
the  pulse-rate  exceeds  150,  though  probably  indicating  a  comparatively 
healthy  ventricle,  does  not  necessarily  imply  a  good  prognosis  (see 
Case  III.). 

When  auricular  flutter  supervenes  in  patients  with  advanced  chronic 
heart  disease,  the  prognosis  is  particularly  unfavourable,  because  the 
change  almost  certainly  indicates  the  extension  of  inflammatory  pro- 
cesses in  the  auricular  walls,  and  also  because  the  acceleration  of  the 
ventricles  increases  still  further  the  insufficiency  of  these  chambers. 
The  flutter  as  a  rule  either  persists  for  weeks  or  mouths,  or  passes  into 
auricular  fibrillation.  In  either  case  there  is  little  probability  of  the 
normal  rhythm  being  restored,  and  in  certain  instances  the  flutter  and 
fibrillation  are  terminal  events. 

In  a  favourable  case,  once  the  attack  has  subsided  and  the  normal 


128  PEOGNOSIS 

cardiac  rhythm  has  been  restored,  the  liabihty  to  recurrence  of  flutter 
is  decidedly  more  pronounced  if  the  patient  has  a  grossly  damaged  heart 
than  if  his  heart  be  apparently  healthy,  because  in  the  former  case  there 
is  the  constant  risk  of  fresh  outbreaks  of  myocarditis.  At  this  stage 
prognosis  will  depend  in  large  measure  upon  the  patient's  habits  and  the 
nature  of  his  occupation.  The  man  or  woman  who  can  lead  a  quiet  life, 
avoiding  physical  strain,  and  who  is  little  subject  to  emotion  and  worry, 
has  the  better  prospect  of  avoiding  subsequent  attacks. 


CHAPTER   XI 

TllEATMENT 

OUK  first  aim  in  the  treatment  of  auricular  flutter  is  the  relief  of  the 
patient's  urgent  symptoms.  This  is  usually  effected  when  the  flutter 
subsides  and  the  physiological  rhythm  is  restored,  or  when  the  ventri- 
cular rate  falls  to  about  the  normal  in  spite  of  the  auricles  continuing 
in  flutter.  Further,  we  have  to  treat  the  causal  condition  whether 
it  be  cardio-vascular  or  nervous,  infective  or  toxic,  structural  or 
functional;  and  lastly,  we  have  to  try  to  prevent  the  recurrence  of 
the  flutter. 

1.  Treatment  during  an  attack  should  be  directed  to  arresting  the 
flutter,  or,  failing  that,  to  lowering  the  excessive  speed  of  the  ventricles. 
Complete  rest  in  bed  is  usually  of  great  benefit  and  is  always  desirable. 
All  unnecessary  physical  exertion  or  strain  should  be  avoided.  In  some 
instances  orthopncea  is  so  pronounced  that  the  patient  cannot  lie  down 
without  aggravating  the  breathlessness ;  but  as  a  rule,  if  there  be  cyan- 
osis, dyspnoea,  or  other  notable  signs  of  heart-failure,  the  patient  should 
be  in  the  recumbent  posture  for  the  greater  part  of  the  day.  It  is  often 
well,  however,  to  permit  him  to  sit  up  in  bed  while  he  is  taking  nourish- 
ment, and  for  about  half  an  hour  afterwards.  Discomfort  due  to  flatulence 
may  thus  be  obviated.  The  patient  should  also  be  shielded  in  so  far  as 
is  possible  from  all  worry,  excitement,  and  emotional  disturbance  which 
might  stimulate  the  accelerator  mechanism  of  his  heart  and  thus  tend 
to  maintain  the  auricular  flutter. 

The  diet  should  be  light  and  digestible,  but  solids  need  not  necessarily 
be  withheld  altogether.  ISTourishment  should  be  given  every  two  or 
three  hours,  so  as  to  avoid  overloading  of  the  stomach  at  any  one  meal. 
Careful  attention  should  be  paid  to  the  state  of  the  bowels,  any  tendency 
to  constipation,  flatulence,  or  diarrhoea  being  corrected  by  appropriate 
dietetic  and  medicinal  measures. 

If  the  patient  is  restless  or  sleepless,  Iromidcs  may  with  benefit  be 
given  in  the  evening.  The  calcium  or  ammonium  salts  are  the  most 
suitable.  In  one  of  Mackenzie's  cases  the  prolonged  administration  of 
ammonium  bromide  in  20-grain  doses  thrice  daily  was  helpful  in  pro- 

129  9 


130  TEEATMENT 

moting  sleep  and  in  checking  the  more  serious  paroxysms  of  ventricular 
acceleration. 

As  the  application  of  an  ice-lag  to  the  precordia  is  sometimes  very 
soothing  to  patients  with  paroxysmal  attacks  of  auricular  fibrillation 
and  other  forms  of  "  paroxysmal  tachycardia,"  it  might  be  well  to  give 
it  a  trial  in  cases  of  auricular  flutter. 

Digital  compression  of  either  the  right  or  left  vagus  may  be  tried. 
In  some  cases  of  "paroxysmal  tachycardia"  this  procedure  has  been 
effective  in  arresting  an  attack,  and  in  auricular  flutter  we  know  that  it 
often  induces  transient  slowing  of  the  ventricles.  In  well-authenticated 
cases  of  auricular  flutter,  however,  the  ventricular  retardation  resulting 
from  vagus-compression  is  of  very  brief  duration ;  the  auricles  mean- 
while continue  in  flutter,  and  within  a  few  seconds  the  high  speed  of  the 
ventricles  is  regained.  Consequently  vagus-compression  can  hardly  be 
regarded  as  having  any  real  therapeutic  value  in  auricular  flutter. 

The  drugs  that  act  most  beneficially  are  digitalis  and  strophanthus. 
It  is  not  necessary  to  administer  these  drugs  in  every  case  of  auricular 
flutter.  Case  IV.,  for  example,  made  a  complete  recovery  without  either 
drug  being  administered.  But  in  most  cases  of  auricular  flutter  the  urgency 
of  the  patient's  symptoms  affords  a  definite  indication  for  the  use  of  one  or 
other  of  these  drugs.  Their  mode  of  action  and  their  remarkable  effects 
have  been  described  in  Chapter  VIII.  It  will  therefore  suffice  to  state 
that  the  initial  effect  of  these  drugs  is  to  lessen  the  rate  of  the  ventricles. 
This  often  falls  to  one-half  of  its  antecedent  rate — for  example,  from  150 
to  75  per  minute — while  the  rhythm  remains  regular.  Subsequently  the 
auricular  flutter  may  become  replaced  by  fibrillation,  and  the  rhythm 
of  the  ventricles  then  becomes  wholly  irregular,  but  their  rate  is  usually 
not  excessive.  In  some  instances  the  normal  rhythm  is  restored  after 
the  digitalis  has  been  withdrawn ;  but  this  successful  result  is  by  no 
means  constantly  attained,  and  we  must  admit  that  the  drug  often  fails 
to  "  make  hearts  beat  our  time  that  flutter  false." 

Although  in  some  instances  the  heart  with  fluttering  auricles  is 
highly  responsive  to  digitalis,  it  is  often  necessary  to  give  this  drug  in 
considerable  doses  for  several  days  before  the  ventricular  rate  falls  and 
the  patient  obtains  relief.  Small  doses,  such  as  five  minims  thrice  daily, 
may  be  of  no  avail.  Twenty  minims  of  digitalis  tincture  should  be 
given  thrice  daily,  and  if  the  ventricular  rate  is  not  retarded  in  the 
course  of  three  or  four  days  the  daily  dose  should  be  increased  to  one 
and  a  half  drachms.  The  tincture  is  usually  effective,  but  other  prepara- 
tions may  be  tried.     Nativelle's  granules  (aio  gr.  of  digitaline,  thrice 


DIGITALIS  131 

daily)  were  given  with  benefit  in  Cases  Y.  and  XIX.,  digalen  was  used 
in  Cases  XV.  and  XVI.,  and  digipuratuni  in  Case  XLII.  If  digitalis 
is  to  be  administered  by  the  mouth,  it  probably  matters  little  which 
preparation  be  employed. 

The  drug  should  be  given  steadily  until,  the  ventricular  rate  having 
fallen  to  about  normal,  the  patient's  urgent  symptoms  are  relieved.  At 
this  stage  the  auricles,  as  a  rule,  are  still  in  flutter.  One  of  two  courses 
may  then  be  followed.  The  daily  amount  of  the  drug  may  be  reduced 
until  the  minimal  dose  that  suffices  to  restrain  the  ventricles  is  beinsr 
given,  and  this  dose  is  continued  for  days,  weeks,  or  months  until  the 
flutter  ceases.  The  alternative  procedure  is  to  maintain  a  large  dose  of 
digitalis  until  the  auricles  pass  into  fibrillation,  and  when  this  event 
supervenes  to  withdraw  the  drug  altogether  for  some  days  in  the  hope 
of  the  normal  cardiac  rhythm  being  restored.  In  most  cases  it  is  neither 
advisable  nor  desirable  to  withhold  the  drug  completely  for  many  days, 
because  the  ventricular  rate  is  apt  to  become  too  frequent,  and  conse- 
quently distressing  symptoms  are  liable  to  recur.  Yet  a  dose  greater 
than  is  sufficient  to  hold  the  ventricles  in  check  is  equally  undesirable, 
for  the  larger  the  dose  of  digitalis  the  less  likelihood  is  there  of  the 
auricular  fibrillation  becoming  replaced  by  a  normal  rhythm. 

Should  we  deliberately  push  the  dose  of  digitalis  until  the  auricles 
are  in  fibrillation,  or  should  we  be  content  with  retarding  the  ventricles 
while  the  auricles  continue  in  flutter  ?  Two  further  problems  arise, 
namely,  what  prospect  is  there  of  the  auricular  fibrillation  that  succeeds 
flutter  being  replaced  by  a  normal  rhythm,  and  how  long  may  the  latter 
be  maintained  ?  The  normal  rhythm  was  restored  in  only  fifteen  out 
of  thirty  cases  treated  with  digitalis,  and  in  one  instance  the  normal 
rhythm  was  apparently  maintained  for  three  years.  Such  a  satisfactory 
result,  however,  is  exceptional,  and  even  after  the  normal  rhythm  has  been 
restored  it  is  liable  to  be  interrupted  from  time  to  time  by  paroxysmal 
attacks  of  flutter  or  fibrillation.  Again,  we  know  that  once  auricular 
fibrillation  is  induced  there  is  a  distinct  tendency  for  it  to  persist.  This 
is  a  most  undesirable  event.  Further,  we  know  that  even  although  the 
auricles  continue  in  flutter  the  patient  may  remain  wonderfully  free  of 
all  distressing  symptoms  provided  his  ventricular  rate  be  not  unduly 
high.  In  Case  II.,  for  example,  the  patient  felt  perfectly  well  when  the 
rate  of  his  ventricles  was  one-fourth  of  the  auricular  rate.  Under  such 
circumstances  the  dose  of  digitalis  should  not  be  increased  with  the 
object  of  inducing  auricular  fibrillation.  On  the  contrary,  the  dose 
should  not  be  larger  than  is  sufficient  to  restrain  the  ventricles.     In 


132  TEEATMENT 

each  case  the  dosage  must  be  determined  by  the  patient's  general 
condition  and  symptoms,  and  in  some  cases  it  may  be  advisable  to 
continue  the  administration  in  small  doses  for  a  long  period,  possibly 
for  years  (see  Case  XVIII.). 

In  spite  of  the  ventricular  rate  having  fallen,  the  patient's  general 
condition  may  not  be  satisfactory.  He  may  still  be  cyanosed,  breathless, 
and  dropsical.  Under  these  circumstances  the  digitalis  should  be  con- 
tinued in  considerable  doses,  and  if  there  be  no  contraindication  it  may 
with  advantage  be  combined  with  caffeine,  diuretin,  theocine,  potassium 
acetate,  or  other  diuretics.  In  my  experience  the  combination  of  digitalis 
with  potassium  iodide  often  acts  remarkably  well"  in  cases  of  chronic 
interstitial  myocarditis.  In  one  case  of  auricular  flutter  this  combina- 
tion was  certainly  helpful.  Mackenzie  ^  is  undoubtedly  correct  in  main- 
taining that  when  digitalis  is  administered  in  therapeutic  doses  it  does 
not  raise  the  arterial  pressure.  Some  cases  of  auricular  flutter,  never- 
theless, show  a  decided  tendency  to  arterial  spasm,  the  hypertonus 
described  by  Eussell.^  This  tendency  should  be  corrected  by  attention 
to  the  patient's  diet,  by  the  administration  of  an  occasional  mercurial 
purge,  and,  if  necessary,  by  the  use  of  nitrites. 

The  action  of  strophanthus  (Cases  III.,  XXIV.,  and  XXV.)  and  of 
squill  (Cases  I.  and  XXXII.)  has  been  investigated  in  only  a  few  cases 
of  auricular  flutter,  but  it  appears  to  be  similar  to  that  of  digitalis. 

When  auricular  flutter  supervenes  late  in  the  course  of  mitral 
disease,  or  when  flutter  is  associated  with  grave  and  urgent  signs  of 
heart  failure,  either  strophanthin  or  some  preparation  of  digitalis  should 
be  given  intravenously.  In  Case  III.,  with  auricular  and  ventricular 
rates  of  320  and  160  per  minute  respectively,  0*001  gramme  of  stroph- 
anthin (Boehringer)  was  given  intravenously  with  great  benefit.  Twelve 
hours  later  the  auricles  were  in  fibrillation,  while  the  ventricular  rate 
had  fallen  to  about  96-104  per  minute,  and  the  patient's  general  con- 
dition had  improved.  On  the  following  day  the  normal  rhythm  of  the 
heart  was  restored,  and  the  rate  was  only  90  per  minute.  In  another 
case  the  intravenous  administration  of  strophanthin  arrested  a  paroxysmal 
attack  which  was  probably  auricular  flutter.  When  the  patient,  an  old 
lady  of  seventy-four,  was  first  seen,  she  was  apparently  dying  of  heart 
failure.  The  extremities  were  cold,  the  pulse-rate  was  150  per  minute, 
and  the  beats  were  very  feeble,  but  they  were  rhythmic  except  for  an 

1  Mackenzie,  J.,  "Digitalis,"  Heart,  Lond.,  1910-11,  ii.,  273. 

2  Russell,  W.,  Arterial  Hypertonus,  Sclerosis,  and  Blood-Pressure,  Edin.  and  Lond., 
1907. 


TREATMENT  133 

occasional  "  intermission."  A  few  hours  after  0*0005  gramme  of  stroph- 
anthin  had  been  given  intravenously  the  patient  began  to  improve,  and 
a  fortnight  later  her  pulse  was  rhythmic,  at  a  rate  of  80  per  minute. 
So  satisfactory  was  the  recovery  that  the  patient  was  able  to  travel  to 
London  about  two  months  later.  Subsequently  the  attacks  of  heart 
failure  recurred  and  became  more  frequent,  and  the  patient  died  seven- 
teen weeks  after  the  initial  attack. 

2.  Treatment  of  the  Causal  Condition.  —  In  the  majority  of  cases, 
auricular  flutter  is  a  result  of  sub-acute  or  chronic  inflammation  of  the 
auricular  musculature.  This  is  often  dependent  upon  disease  of  the 
valves  or  of  the  pericardium,  or  still  more  frequently  upon  arterio- 
sclerosis. All  these  causal  factors  should  be  borne  in  mind  in  treating 
a  case  of  auricular  flutter.  A  history  of  rheumatism  or  of  syphilis  may 
yield  a  clue  to  appropriate  and  successful  treatment. 

3.  The  Prevention  of  Becicrrent  Attacks.  —  Success  or  failure  in  the 
treatment  of  each  case,  during  an  attack  or  after  it  has  subsided,  is 
largely  dependent  upon  our  ability  to  treat  the  underlying  cause. 
Although  a  pre-existing  mitral  stenosis  cannot  be  abolished,  or  thickened 
coronary  arteries  be  replaced  by  healthy  vessels,  much  may  be  done  to 
check  the  further  progress  of  the  disease.  The  patient  should  be  advised 
regarding  his  general  mode  of  life.  He  should  be  directed  to  relinquish 
his  arduous  occupation  for  one  that  entails  little  physical  or  mental 
strain.  The  amount  of  physical  exercise  or  intellectual  work  that  he 
may  undertake  daily  without  risk  to  his  health  should  be  indicated,  and 
any  tendency  to  indiscretion  in  food,  drink,  or  tobacco  should  be  corrected. 
By  attention  to  any  obvious  or  latent  sources  of  infection,  whether  in  the 
alimentary  tract  or  elsewhere,  the  risk  of  the  myocardium  becoming  re- 
infected may  be  lessened.  By  these  measures  we  strive  to  prevent  the 
paroxysmal  attacks  from  recurring,  and  even  although  in  some  cases  we 
realise  that  our  efforts  are  foredoomed  to  failure,  in  others  we  may  hope 
for  no  small  measure  of  success. 


GENERAL    INDEX 


, 

I'AOE 

a  WAVE        ...... 

6 

a-c  interval               ..... 

6 

Abdominal  pain     ..... 

46,  78,  8.0 

viscera              ..... 

30,  33,  46,  62,  85 

Adams-Stokes  syndrome    .... 

37,  89 

Age  incidence          ..... 

.       28 

Air  swallowing       ..... 

.       75 

Albuminutia           ..... 

42,  46,  59,  78,  85 

Alcoholism              ..... 

.       56,  65,  72 

Alternation  of  pulse,  after  vagus  compression 

.     102 

in  auricular  Hutter      .... 

.      47,  62, 

73,  76,  90,  92,  127 

Amyl  nitrite           ..... 

.       39 

Aortic  incompetence,  electrocardiogram  in 

.       11 

flutter  and            .... 

29,  79 

valve  in  flutter             .... 

30,  32 

Aortitis,  syphilitic  ...... 

17,  74 

Arterial  pressure    ..... 

29,  81 

pulse.     See  Pulse. 

Arterio-sclerosis,  extrasy  stoles  in  . 

.       16 

flutter  and       ..... 

29,  64 

As  —  Vs  interval  in  flutter .... 

.     123 

in  nodal  extrasystoles 

.       15 

normal             ..... 

.  6,  15 

Atrio-ventricular  bundle,  branches  of 

.        4,  31, 

33,  34,  74,  89,  120 

in  auricular  fibrillation 

22 

in  case  with  auricular  extrasystoles    . 

.       17 

in  complete  heart-block 

88,  89 

in  flutter          ..... 

30 

31,  33,  34,  77,  87 

in  nodal  rhythm          .... 

116,  119 

site  of  . 

4 

structure  of     . 

4 

Atrio-ventricular  node,  in  case  with  auricular  extras 

vstoles 

.       17 

in  flutter          ..... 

31,  33,  34,  77 

in  nodal  rhythm          .... 

116,  117,  119 

site  and  structure  of    . 

3 

Atropin       ...... 

28,  38, 

40,  43,  66,  72,  88 

effects  on  auricles        .... 

.       97 

Auricles,  lesions  of,  in  fibrillation 

.       22 

in  flutter          ..... 

28,  30,  31,  32,  .33 

Auricular  deflexions,  diphasic 

10, 

43,  48,  49,  93,  99 

in  fibrillation  ..... 

.       21 

in  flutter          ..... 

42,  43,  57,  93 

in  nodal  rhythm          .... 

119,  120 

in  vagus  stimulation  .... 

.       99 

inverted           ..... 

10,  15,  103,  121 

135 


136 


GENEEAL  INDEX 


Auricular  extrasystoles,  morbid  anatomy  of  case  with 

prognosis  in  cases  with 
Auricular  rate  in  flutter    . 


b  WAVE 

Bathmotropic  influences 
Belladonna 

See  also  Atropin. 
Blood -pressure 
Bieathlessness 
Bromides     . 
Bronchitis  . 


Carotid  impulse    . 

Cases,  records  of 

Cheyne-Stokes  breathing 

Chloroform  anaesthesia 

Chronotropic  influences 

Clinical  features     . 

Combined  flutter  and  fibrillation 

Conducting  system.     See  Atrio-vextricular  B 

Conduction  of  stimuli 

in  auricles,  defective  . 

in  flutter 

vagus  influence  on 
Contractility  of  auricles,  vagus  effect  on 

of  ventricles,  vagus  effect  on 
Coronary  arteries  in  flutter 

artery,  occlusion  of  left 

sinus  in  flutter 
stimiilation  of 
Cyanosis 


Death 
Delirium     . 
Diagnosis    . 

from  auricular  fibrillation 

extrasystolic  arrhythmia 

nodal  rhythm     . 

physiological  rhythm 

sinus  tachycardia 
Digitalin 
Digitalis 

heart-block,  atropin  in 
Diphtheria . 
Diuretin 

Dromotropic  influences 
Dropsy        .  .  .  .  52,  63 

Duration  of  auricular  flutter 
Dyspnoea 


16,  17 
.  16 
24,93 

7 
.  95 
.      79 

29,81 

83,  84,  85 

.     129 

79,  84 


6 

35-80 
59,  74,  76,  85 

29,  62 
.       95 

81-89 
26,  27,  28,  56,  57,  93,  94,  104,  124 

UNDLE   AND   NODE. 

12,  95 
23,  100 

25,  87,  104,  105 

100,  101 

.       99 

102,  104 

30,  33 
.  17 
.  33 
.       28 

67,  68,  69,  70,  72,  74,  82,  85 


54,  59,  64,  65,  70,  74,  75,  76,  77, 


64,  66 


Electrocardioc4Ram  of  auricular  fibrillation 
of  extrasystoles 


67,  68 


71,  72 


86,  127 
75,  85 
111-125 
122 
114 
115 
111 
113 

56,  72,  91,  130 

106-110,  130-132 

.   98 

29,  33,  34,  70,  76,  77 

52,  64,  66,  132 

.   95 

73,  74,  76,  79,  80,  85 

84,  126 

83,  84,  85 

.  21,  93,  124 
.   14,  15,  115 


GENEEAL  INDEX 


137 


Electrocardiogi-am  of  flutter 

of  nodal  rhj'thm 

of  normal  heart 

of  sinus  tachycardia 
Electrocardiograph 
Electrocardiographic  deflexions 

derivations 
Emotion,  influence  of 
Endocarditis 
Etiology 
Excitability 

of  auricles 

of  ventricles    . 
Exciting  causes 
Exophthalmic  goitre 
Experimental  production  of  flutte 
Extrasystoles 

after  flutter 

before  flutter  . 

flutter  simulating 

multiple 

relation  to  flutter  and  fibrillation 

significance  of 

supra-ventricular 

vagus  influence  on 

varieties  of 

ventricular,  in  flutter 
Extrasystolic  arrhythmia 

Faixtxess 

Fatty  degeneration  of  heart 
Fibrillation,  auricular 

chloroform  antesthesia  and 

combined  with  flutter 

death  from 

defective  conductivity  as  cause  of 

diagnosis  from  flutter 

digitalis  and    . 

dilatation  of  heart  in 

electrocardiogram  in 

following  flutter 

jugular  pulse  in 

myocarditis  and 

paroxysmal 

persistent 

pulse  in 

relation  to  flutter 

symptoms  of    . 
"  Fluttering,"  sensation  of , 

Galvanometer  fibre,  deflexion  of 

tension  of         . 
Galvanometric  curves.    See  Electrocardiogram 
Ganglia       ...... 


42-45,  47,  53,  55,  57,  64,  93,  94 
119-121 
9 
.     114 
8 
.  9,  10 
9 
28,  71,  75,  84,  105 
31,  117 
.       24 
12,  95 
.       98 
.     104 
82,  84 
29,  32,  60,  113 
24-27,  110 
12-17 
73,  79,  107 
60,  76,  82 
.     114 
16,  23,  29,  82,  115 
22,  23 
.       16 
14,  15,  16,  23,  60,  107,  114 
.     101 
.       14 
44,  92 
.     114 

52,  5o,  73,  78,  84 

33,  34,  69,  77 

17-23,  122-125 

.       29 

26,  27,  28,  56,  57,  93,  94,  124 

17,  20 

23,  100 

122-125 

21,  106,  108,  130,  131 

.       20 

21,  93,  124 

86,  106,  108,  125,  131 

.       21 

.       22 

.       18 

.       20 

.     123 

22,  23 

.  19-21 

67,  82 

.     8,  9 
9 

3,  26  31 


138 


GENERAL   INDEX 


Gastro-intestinal  catarrh 

Gout 

Graphic  records 

h  WAVE 

Heart-block,  atropin  in 

complete 

partial 

vagus  stimulation  and 
Heart  disease  and  flutter 
Heart  failure,  extrasystoles 

flutter  in 
Heart-sound,  third 
Heart-sounds  in  flutter 

electrocardiographic  deflexions  and 
Heterotopic  stimulus 
Hypertonus,  arterial 

Ice-bag 

Infection,  acute 

Influenza    . 

Inhibition  of  ventricles  in  flutter 

Inhibitory  area 

Inotropic  influences 

Insomnia    . 

Iodides 

Ipecacuanha 


Jaundice   . 
Jugular  veins,  analysis  of  tracing; 
.  pulsations  of    . 

in  extrasystoles 

in  fibrillation 

in  flutter . 

in  nodal  rhythm 

in  sinus  tachycardia 

Liver,  congestion  of 
LymphocythfBmia  . 

Mediastino-pericarditis 
Mercury 

Mitral  disease,  fibrillation  and 
flutter  and 

incompetence  . 

stenosis 

electrocardiogram  in 
Morbid  anatomy     . 
Murmurs,  disappearance  of 
Myocarditis 

in  fibrillation  . 
Myogenic  theory     . 


from 


29, 


29, 


42, 


PAGE 

29,  79,  82 

.       71 

90-94 

7,  93,  112 

.       98 

35,  37,  88,  89 

65,  86 

88,  101 

84 

16 

84-86 

7 

83,  85 

10 

13 

132 

130 

74 

62,  70,  73,  82 

26,  104 

.       25 

.       95 

59,  62,  84,  129 

51,  132 

.       75 

54,  65,  85 

6 

4 

.       14 

21,  123,  124 

47,  53,  92,  93 

118,  119 

113 


.       85 
.       69 

16,36 
.       51 
.       18 
29,  66,  84 
36,  46,  64,  72,  77 
30,  51,  56,  77,  85 
11 
30-34 
.     79,  85,  114 
31,  32,  74,  77,  84,  133 
.       22 
.       12 


GENERAL   INDEX 


139 


N'AUSEA        ...... 

.       79 

Nephritis,  acute      ..... 

.       77 

chronic            ..... 

76,  84 

Nerves  in  atrio-ventricular  node  ami  IhuiiUl' 

4 

in  inhibitory  area        .... 

.       26 

in  sinus  node  ..... 

.  3,31 

Neurogenic  theory             .... 

.       12 

Nitrites      ...... 

,39,  46,  48,  132 

Nodal  extrasystoles            .... 

14,  15 

rhythm           ..... 

76,  77,  115-122 

Node.    .See  Atrio-vextricular  and  Sinus. 

Normal  rhythm  of  auricles  regained 

84,  86,  126,  131 

in  experimental  flutter 

26,  104,  108-110 

(Edema.     See  Drop.sy. 

Opium         ...... 

.       79 

Orthodiagrams,  auricular  fibrillation 

20,  50 

Hutter  and  heart-block 

.       36 

normal  heart  ..... 

.       20 

F  DEFLEXION,  diphasic       .... 

10,  43,  48,  93 

inverted           ..... 

10,  15,  103,  121 

normal             ..... 

9 

Pain 46, 

68,  69,  71,  78,  79,  80,  83,  84 

Palpitation             ..... 

83,  84 

Pause  after  extrasystole     .... 

.       14 

after  fibrillation           .... 

.     109 

after  flutter      ..... 

109,  110 

Persistence  of  flutter           .... 

.     27,  86,  126 

Pericarditis             ..... 

.       30 

Pneumonia              ..... 

73,  77 

Polygraph,  Mackenzie's     .            .            .            . 

5 

tracings.     See  Jugular  Veix.s. 

Posture,  eftect  of     . 

76,  85,  112,  122 

Primitive  tissue      ..... 

2 

Prognosis    ...... 

126-128 

Prostration              ..... 

83,  84 

Pulse,  arterial,  in  fibrillation 

.     123 

in  flutter ..... 

83,  85,  90 

venous.    See  Jugular  Veins. 

Pulsus  alternans.     See  Alternation  of  Pulse. 

Purkinje  fibres       ..... 

4 

Q  deflexion          ..... 

9 

R  deflexion  in  flutter      .... 

.       94 

normal              ..... 

9 

Recovery     ...... 

84,  126 

Refractory  phase    ..... 

.       12 

Respiration,  flutter  and     .... 

.     112 

jugular  pulsations  and 

5 

Rheumatism           ..... 

29,  51,  56,  69,  75,  133 

140 


GENEEAL  INDEX 


;S'  DEFLEXION  ill  flutter 

normal 
Sex  incidence 

Sino-auricular  node.     See  Sinus 
Sinus  extrasystoles 
Sinus  node,  destruction  of 

in  fibrillation  . 

in  flutter 

site  of  . 

stimulus  production  in 

structure  of 
Sinus  tachycardia  . 
Somnolence 
Spliygmograms 
Squill 
Stimulus  production 

in  flutter 
Strophanthin 
Stropliantlius 
Stupor 
Supra-ventricular  extrasystoles 

relation  to  flutter 
Sympathetic  action,  in  flutter 
on  normal  heart  . 

sj'stem  in  flutter 
Symptoms  . 

premonitory    . 
Syncope 
Syphilis 

T  DEFLEXION 

Tone  ... 

Tonicity.     See  Tone. 
Tonotropic  influences 
Tonsillitis  .  .  .        • 

Tracings  from  jugular  veins.     Bee 
Treatment  . 
Tremor  cordis 


Unconsciousness  . 

V  WAVE 

in  sinus  tachycardia    . 
Vagi,  section  of 
Vagus,  action  of 

in  auricular  flutter 

on  auricles 

on  conducting  system 

on  extrasystoles  . 

on  ventricles 
compression  of 

in  flutter  43,  47,  48,  49,  53,  55,  57,  66,  67,  70,  71,  79, 

in  treatment         .  .  .  ... 


Jugular  Vein 


PAGE 

.   94 

9 

.   29 

14,  15 
.   28 
.   22 
31,  33,  34,  77 
3 
.   12 
3 
113,  114 
65,  85 
.   90 
39,  73,  108 
12,  95 
28,  93 
40,  43,  53,  107,  132 
41,  52,  62,  70,  107 
74,  85 
14,  15,  16,  60,  107,  114 
.   23 
.  105 
.  103 
.   33 
81-89 
.   82 
58,  75,  83,  84 
17,  29,  45,  74,  133 


9 
95,  101 


.   95 

29,80 

129-133 
.   82 

75,  84 

.6,7 
.  113 

28,  99 

95-105 

103-105 

.   97 

101,  104 
.  101 

102,  104 
.   96 

103-104,  123 
.  130 


GENEEAL   INDEX 


141 


Vagus,  faradisation  of 

inhibition,  escape  from 
nerves  in  flutter 
stimulation,  after-effects  of 

electrocardiogi-am  during 

flutter  and 

heart-block  and  . 
Ventricles,  coupled  beats  (jf 
group-beating  of 
hypertrophy  of 
in  experimental  flutter 
in  fibrillation  . 
in  flutter 

irregularity  of,  in  flutter 
rate  of,  in  flutter 

in  heart-block 
retardation  of . 
Ventricular  deflexions 

atypical    . 

in  extrasystoles   . 

in  flutter  . 

in  nodal  rhythm . 
diastole,  duration  of   . 
extrasystoles   . 
systole,  duration  of     . 
venous  pulse    . 
Vertigo 
Vomiting  arrests  attacks    . 

AVA.s.SERMA>rx  reaction 

X  DEPRESSION 
IJ  DEPRESSION 


PAGE 

104,  no 

.  102 
30,  33 
.  102 

11,  97,  99,  100,  101,  103,  104 
57,  103-105,  108-110 
.  88 
87,  106 
44,  58,  76,  90 
11,  94 
.  25 
17-22 
44,  81-94,  106,  107 
,  48,  55,  56,  65,  90,  106,  122 
25,  83,  85,  90 
.  88 
26,  104,  106,  108 
.  10 
14,  50 
14,  15 
.  94 
116,  119 
.  81 
.  14,  50,  114 
.  81 
21,  47,  53,  64,  93,  124 
55,  72,  78,  79,  83 
75 

35,  79 

.     .    6 

6 


INDEX   OF    AUTHORS 


Adami,  J.  G. 

Balfour,  G.  W. 
Bamberger,  H. 
Bayliss,  W.  M. 
Belski,  a. 
Blacoian,  J.  R. 

BOWDITCH,  H.  p. 

Bull,  L.   . 

CoHX,  A.  E. 
Cowan,  J. 
cushnt,  a.  r. 
czermak,  j.  n. 

Draper,  G. 

Edmunds,  C.  W. 
Einthoven,  W. 
Engelmann,  Th.  W. 
Eppinger,  H. 
Erlanger,  J. 
Eyster,  J.  a.  E. 

Fahr,  G.  . 
Fahrenkamp,  K 
Flack,  M. 
Fleming,  G.  B. 
Fowler,  W.  Hope 
Fredericq,  L. 
Friedreich,  N. 
Fulton,  F.  T. 

Galen 

Gaskell,  W.  H. 
Geigel,  a. 
Gibson,  A.  G. 
Gibson,  G.  A. 

GOODHART,  G.  W. 

Gunk,  J.  D. 

Hart,  T.  Stuart 
Hay,  J.     . 
Hecht,  a.  F. 


PAGE 

96 

82 
1 
96 
117 
45 
12 
10 


103 

35,  78,  79,  117 

17,  109,  116 

96 

22,  96 

17 

2,  8,  9,  96,  97,  99,  100 
27,96 
120 
45,  117 
101 

10 
77 

2 

117 

20 

17 

1 
76 


12,  27,  45,  96,  98,  100,  101 
1 
7 

1,  30,  35,  37,  65,  82,  87,  88 
66,87 
10 

.       115 

72,  73,  108 
29,  117 


142 


INDEX   OF   AUTHOES 


143 


Hedinger,  E. 
Hering,  H.  E. 
Hertz,  A.  F. 
Hirschfelder,  a.  D. 
His,  W.,  Jr. 
Hoffmann,  A. 
Hume,  W.  E. 

Jolly,  W.  A. 

Kahn,  R.  H. 
Keith,  A. 
Kennedy,  A.  M. 
Kent,  A.  F.  S. 
Koch,  W.  . 
korteweg,  a.  j. 

Laslett,  E.  E. 
Lea,  C.  E. 
Lewis,  T.  . 
Levy,  A.  G. 
Lohmann,  a. 
Loven, 

Macpiarmid,  p. 
Mackenzie,  J. 
Mac  William,  J.  A 
Marey,  E.  J. 
Mathewson,  G.  D 
Meek,  W.  J. 
Meiklejohn,  J. 
morgagni,  j.  b. 
Morison,  a. 
muskens,  l.  j.  j 

Nobel,  E. 

Philips,  F. 

Radasewsky,  M. 

RiEGEL,  F. 
RlHL,  J.      . 

Robinson,  G.  Canby 
rothberger,  c.  j. 
Roy,  C.  S. 
Russell,  W. 


schleiter,  h.  g. 
Schonberg,  S. 
Starling,  E.  H. 
Stoerk,  O. 
Stokes,  W. 
Stromberg 


10,  la 


1,  2,  5, 


67,  68 


69,  70, 


PAOE 

22 

17,96,  116 

.  66,  87 

.  7,  26 

4 

24,  79,  80,  115,  117,  121 
33,  72,  76,  77,  108,  112,  118 

.  18,  24,  35,  42 

10,  99 

2 

117 

4 

22 

26,  107,  108 

97 

.  68,  69 
71,  72,  87,  100,  109,  117,  121 
29 
116 
27 


15,  58,  67,  71,  73,  74,  75,  84,  129,  132 
17,  24,  25,  26,  27,  96,  100,  101,  104 
.  1,14 
77,  120 
.  101 
.  3,4 
1 
.  24,  65 
.   101 

29 

17 

22 

1 

24,  66,  67,  108,  116,  117 

24,  26,  27,  94,  96,  104 

18,  26,  97,  99,  103,  117,  119,  121 

96 


£7U 

.       132 

68 

22 

96 

.       120 

1 

27 

144                               INDEX  OF  AUTHORS 

PAGE 

Tawara,  S.           .            .            .  •  •            •  •  •  .3 

TiGERSTEDT              .                .                 •  •  '        •                •  •  '        •  .27 

TuRNBULL,  H.  Hume       .            .  .  •            •  •  •  .67 

ViXNIS,  E.  W.  GOTELING                 .  .  .               .  .  ■  .72 

Waller,  A.  D.     . 


Watson-Wemyss,  H.  L. 
Wenckebach,  K.  F. 
WiERINGA,  J.  H.   . 
Winterberg,  H. 

Zahn,  a.  . 


10 

.     2,  45,  95,  97 

96 

18,  26,  97,  99,  100,  103,  117,  119,  121 


28 


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